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Published in: Current Heart Failure Reports 4/2017

Open Access 01-08-2017 | Comorbidities of Heart Failure (C Angermann and F Edelmann, Section Editors)

Inflammation – Cause or Consequence of Heart Failure or Both?

Authors: Sophie Van Linthout, Carsten Tschöpe

Published in: Current Heart Failure Reports | Issue 4/2017

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Abstract

Purpose of Review

With the intention to summarize the currently available evidence on the pathophysiological relevance of inflammation in heart failure, this review addresses the question whether inflammation is a cause or consequence of heart failure, or both.

Recent Findings

This review discusses the diversity (sterile, para-inflammation, chronic inflammation) and sources of inflammation and gives an overview of how inflammation (local versus systemic) can trigger heart failure. On the other hand, the review is outlined how heart failure-associated wall stress and signals released by stressed, malfunctioning, or dead cells (DAMPs: e.g., mitochondrial DNA, ATP, S100A8, matricellular proteins) induce cardiac sterile inflammation and how heart failure provokes inflammation in various peripheral tissues in a direct (inflammatory) and indirect (hemodynamic) manner. The crosstalk between the heart and peripheral organs (bone marrow, spleen, gut, adipose tissue) is outlined and the importance of neurohormonal mechanisms including the renin angiotensin aldosteron system and the ß-adrenergic nervous system in inflammation and heart failure is discussed.

Summary

Inflammation and heart failure are strongly interconnected and mutually reinforce each other. This indicates the difficulty to counteract inflammation and heart failure once this chronic vicious circle has started and points out the need to control the inflammatory process at an early stage avoiding chronic inflammation and heart failure. The diversity of inflammation further addresses the need for a tailored characterization of inflammation enabling differentiation of inflammation and subsequent target-specific strategies. It is expected that the characterization of the systemic and/or cardiac immune profile will be part of precision medicine in the future of cardiology.
Literature
1.
go back to reference Ponikowski P, Voors AA, Anker SD, Bueno H, Cleland JG, Coats AJ, et al., M. Authors/Task Force, R. Document. ESC guidelines for the diagnosis and treatment of acute and chronic heart failure: the task force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC). Developed with the special contribution of the Heart Failure Association (HFA) of the ESC. Eur J Heart Fail. 2016;2016(18):891–975. Ponikowski P, Voors AA, Anker SD, Bueno H, Cleland JG, Coats AJ, et al., M. Authors/Task Force, R. Document. ESC guidelines for the diagnosis and treatment of acute and chronic heart failure: the task force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC). Developed with the special contribution of the Heart Failure Association (HFA) of the ESC. Eur J Heart Fail. 2016;2016(18):891–975.
2.
go back to reference Borlaug BA, Paulus WJ. Heart failure with preserved ejection fraction: pathophysiology, diagnosis, and treatment. Eur Heart J. 2011;32:670–9.PubMedCrossRef Borlaug BA, Paulus WJ. Heart failure with preserved ejection fraction: pathophysiology, diagnosis, and treatment. Eur Heart J. 2011;32:670–9.PubMedCrossRef
3.
go back to reference Packer M. The neurohormonal hypothesis: a theory to explain the mechanism of disease progression in heart failure. J Am Coll Cardiol. 1992;20:248–54.PubMedCrossRef Packer M. The neurohormonal hypothesis: a theory to explain the mechanism of disease progression in heart failure. J Am Coll Cardiol. 1992;20:248–54.PubMedCrossRef
4.
go back to reference Seta Y, Shan K, Bozkurt B, Oral H, Mann DL. Basic mechanisms in heart failure: the cytokine hypothesis. J Card Fail. 1996;2:243–9.PubMedCrossRef Seta Y, Shan K, Bozkurt B, Oral H, Mann DL. Basic mechanisms in heart failure: the cytokine hypothesis. J Card Fail. 1996;2:243–9.PubMedCrossRef
5.
go back to reference Westermann D, Lindner D, Kasner M, Zietsch C, Savvatis K, Escher F, et al. Cardiac inflammation contributes to changes in the extracellular matrix in patients with heart failure and normal ejection fraction. Circ Heart Fail. 2011;4:44–52.PubMedCrossRef Westermann D, Lindner D, Kasner M, Zietsch C, Savvatis K, Escher F, et al. Cardiac inflammation contributes to changes in the extracellular matrix in patients with heart failure and normal ejection fraction. Circ Heart Fail. 2011;4:44–52.PubMedCrossRef
6.
go back to reference • Paulus WJ, Tschope C. A novel paradigm for heart failure with preserved ejection fraction: comorbidities drive myocardial dysfunction and remodeling through coronary microvascular endothelial inflammation. J Am Coll Cardiol. 2013;62:263–71. This novel paradigm postulated for heart failure with preserved ejection fraction (HFpEF) proposes a central role for endothelial inflammation induced by comorbidities in HFpEF-associated cardiac remodeling. • Paulus WJ, Tschope C. A novel paradigm for heart failure with preserved ejection fraction: comorbidities drive myocardial dysfunction and remodeling through coronary microvascular endothelial inflammation. J Am Coll Cardiol. 2013;62:263–71. This novel paradigm postulated for heart failure with preserved ejection fraction (HFpEF) proposes a central role for endothelial inflammation induced by comorbidities in HFpEF-associated cardiac remodeling.
7.
go back to reference •• Libby P, Nahrendorf M, Swirski FK. Leukocytes link local and systemic inflammation in ischemic cardiovascular disease: an expanded “cardiovascular continuum”. J Am Coll Cardiol. 2016;67:1091–103. This review provides new insights into the integrative biology of inflammation as it contributes to ischemic cardiovascular disease, including unsuspected inflammatory signaling networks that link the brain, autonomic nervous system, bone marrow, and spleen to the atherosclerotic plaque and to the infarcting myocardium. •• Libby P, Nahrendorf M, Swirski FK. Leukocytes link local and systemic inflammation in ischemic cardiovascular disease: an expanded “cardiovascular continuum”. J Am Coll Cardiol. 2016;67:1091–103. This review provides new insights into the integrative biology of inflammation as it contributes to ischemic cardiovascular disease, including unsuspected inflammatory signaling networks that link the brain, autonomic nervous system, bone marrow, and spleen to the atherosclerotic plaque and to the infarcting myocardium.
8.
go back to reference Dick SA, Epelman S. Chronic heart failure and inflammation: what do we really know? Circ Res. 2016;119:159–76.PubMedCrossRef Dick SA, Epelman S. Chronic heart failure and inflammation: what do we really know? Circ Res. 2016;119:159–76.PubMedCrossRef
9.
go back to reference Heymans S, Hirsch E, Anker SD, Aukrust P, Balligand JL, Cohen-Tervaert JW, et al. Inflammation as a therapeutic target in heart failure? A scientific statement from the Translational Research Committee of the Heart Failure Association of the European Society of Cardiology. Eur J Heart Fail. 2009;11:119–29.PubMedPubMedCentralCrossRef Heymans S, Hirsch E, Anker SD, Aukrust P, Balligand JL, Cohen-Tervaert JW, et al. Inflammation as a therapeutic target in heart failure? A scientific statement from the Translational Research Committee of the Heart Failure Association of the European Society of Cardiology. Eur J Heart Fail. 2009;11:119–29.PubMedPubMedCentralCrossRef
11.
go back to reference Torre-Amione G, Kapadia S, Lee J, Durand JB, Bies RD, Young JB, et al. Tumor necrosis factor-alpha and tumor necrosis factor receptors in the failing human heart. Circulation. 1996;93:704–11.PubMedCrossRef Torre-Amione G, Kapadia S, Lee J, Durand JB, Bies RD, Young JB, et al. Tumor necrosis factor-alpha and tumor necrosis factor receptors in the failing human heart. Circulation. 1996;93:704–11.PubMedCrossRef
12.
go back to reference Vasan RS, Sullivan LM, Roubenoff R, Dinarello CA, Harris T, Benjamin EJ, et al. Inflammatory markers and risk of heart failure in elderly subjects without prior myocardial infarction: the Framingham Heart Study. Circulation. 2003;107:1486–91.PubMedCrossRef Vasan RS, Sullivan LM, Roubenoff R, Dinarello CA, Harris T, Benjamin EJ, et al. Inflammatory markers and risk of heart failure in elderly subjects without prior myocardial infarction: the Framingham Heart Study. Circulation. 2003;107:1486–91.PubMedCrossRef
13.
go back to reference Edelmann F, Holzendorf V, Wachter R, Nolte K, Schmidt AG, Kraigher-Krainer E, et al. Galectin-3 in patients with heart failure with preserved ejection fraction: results from the Aldo-DHF trial. Eur J Heart Fail. 2015;17:214–23.PubMedCrossRef Edelmann F, Holzendorf V, Wachter R, Nolte K, Schmidt AG, Kraigher-Krainer E, et al. Galectin-3 in patients with heart failure with preserved ejection fraction: results from the Aldo-DHF trial. Eur J Heart Fail. 2015;17:214–23.PubMedCrossRef
14.
go back to reference Bozkurt B, Torre-Amione G, Warren MS, Whitmore J, Soran OZ, Feldman AM, et al. Results of targeted anti-tumor necrosis factor therapy with etanercept (ENBREL) in patients with advanced heart failure. Circulation. 2001;103:1044–7.PubMedCrossRef Bozkurt B, Torre-Amione G, Warren MS, Whitmore J, Soran OZ, Feldman AM, et al. Results of targeted anti-tumor necrosis factor therapy with etanercept (ENBREL) in patients with advanced heart failure. Circulation. 2001;103:1044–7.PubMedCrossRef
15.
go back to reference Anker SD, Coats AJ. How to recover from renaissance? The significance of the results of recover, renaissance, renewal and attach. Int J Cardiol. 2002;86:123–30.PubMedCrossRef Anker SD, Coats AJ. How to recover from renaissance? The significance of the results of recover, renaissance, renewal and attach. Int J Cardiol. 2002;86:123–30.PubMedCrossRef
16.
17.
go back to reference G. Majno, I. Joris, Cells, Tissues, and Disease., Second Edition ed., Oxford University Press 2004. G. Majno, I. Joris, Cells, Tissues, and Disease., Second Edition ed., Oxford University Press 2004.
19.
go back to reference J.S. Bezbradica, R.C. Coll, K. Schroder, Sterile signals generate weaker and delayed macrophage NLRP3 inflammasome responses relative to microbial signals, Cell Mol Immunol, (2016). J.S. Bezbradica, R.C. Coll, K. Schroder, Sterile signals generate weaker and delayed macrophage NLRP3 inflammasome responses relative to microbial signals, Cell Mol Immunol, (2016).
20.
22.
go back to reference Franks PW, McCarthy MI. Exposing the exposures responsible for type 2 diabetes and obesity. Science. 2016;354:69–73.PubMedCrossRef Franks PW, McCarthy MI. Exposing the exposures responsible for type 2 diabetes and obesity. Science. 2016;354:69–73.PubMedCrossRef
23.
go back to reference Lindner D, Zietsch C, Tank J, Sossalla S, Fluschnik N, Hinrichs S, et al. Cardiac fibroblasts support cardiac inflammation in heart failure. Basic Res Cardiol. 2014;109:428.PubMedCrossRef Lindner D, Zietsch C, Tank J, Sossalla S, Fluschnik N, Hinrichs S, et al. Cardiac fibroblasts support cardiac inflammation in heart failure. Basic Res Cardiol. 2014;109:428.PubMedCrossRef
24.
go back to reference Van Linthout S, Miteva K, Tschope C. Crosstalk between fibroblasts and inflammatory cells. Cardiovasc Res. 2014;102:258–69.PubMedCrossRef Van Linthout S, Miteva K, Tschope C. Crosstalk between fibroblasts and inflammatory cells. Cardiovasc Res. 2014;102:258–69.PubMedCrossRef
25.
go back to reference Sandanger O, Ranheim T, Vinge LE, Bliksoen M, Alfsnes K, Finsen AV, et al. The NLRP3 inflammasome is up-regulated in cardiac fibroblasts and mediates myocardial ischaemia-reperfusion injury. Cardiovasc Res. 2013;99:164–74.PubMedCrossRef Sandanger O, Ranheim T, Vinge LE, Bliksoen M, Alfsnes K, Finsen AV, et al. The NLRP3 inflammasome is up-regulated in cardiac fibroblasts and mediates myocardial ischaemia-reperfusion injury. Cardiovasc Res. 2013;99:164–74.PubMedCrossRef
28.
go back to reference Spillmann F, Van Linthout S, Miteva K, Lorenz M, Stangl V, Schultheiss HP, et al. LXR agonism improves TNF-alpha-induced endothelial dysfunction in the absence of its cholesterol-modulating effects. Atherosclerosis. 2014;232:1–9.PubMedCrossRef Spillmann F, Van Linthout S, Miteva K, Lorenz M, Stangl V, Schultheiss HP, et al. LXR agonism improves TNF-alpha-induced endothelial dysfunction in the absence of its cholesterol-modulating effects. Atherosclerosis. 2014;232:1–9.PubMedCrossRef
29.
go back to reference Spillmann F, Miteva K, Pieske B, Tschope C, Van Linthout S. High-density lipoproteins reduce endothelial-to-mesenchymal transition. Arterioscler Thromb Vasc Biol. 2015;35:1774–7.PubMedCrossRef Spillmann F, Miteva K, Pieske B, Tschope C, Van Linthout S. High-density lipoproteins reduce endothelial-to-mesenchymal transition. Arterioscler Thromb Vasc Biol. 2015;35:1774–7.PubMedCrossRef
30.
go back to reference Spillmann F, De Geest B, Muthuramu I, Amin R, Miteva K, Pieske B, et al. Apolipoprotein A-I gene transfer exerts immunomodulatory effects and reduces vascular inflammation and fibrosis in ob/ob mice. J Inflamm (Lond). 2016;13:25.CrossRef Spillmann F, De Geest B, Muthuramu I, Amin R, Miteva K, Pieske B, et al. Apolipoprotein A-I gene transfer exerts immunomodulatory effects and reduces vascular inflammation and fibrosis in ob/ob mice. J Inflamm (Lond). 2016;13:25.CrossRef
31.
go back to reference Van Linthout S, Spillmann F, Lorenz M, Meloni M, Jacobs F, Egorova M, et al. Vascular-protective effects of high-density lipoprotein include the downregulation of the angiotensin II type 1 receptor. Hypertension. 2009;53:682–7.PubMedCrossRef Van Linthout S, Spillmann F, Lorenz M, Meloni M, Jacobs F, Egorova M, et al. Vascular-protective effects of high-density lipoprotein include the downregulation of the angiotensin II type 1 receptor. Hypertension. 2009;53:682–7.PubMedCrossRef
33.
go back to reference Odeberg J, Freitag M, Forssell H, Vaara I, Persson ML, Odeberg H, et al. Influence of pre-existing inflammation on the outcome of acute coronary syndrome: a cross-sectional study. BMJ Open. 2016;6:e009968.PubMedPubMedCentralCrossRef Odeberg J, Freitag M, Forssell H, Vaara I, Persson ML, Odeberg H, et al. Influence of pre-existing inflammation on the outcome of acute coronary syndrome: a cross-sectional study. BMJ Open. 2016;6:e009968.PubMedPubMedCentralCrossRef
34.
go back to reference Kindermann I, Kindermann M, Kandolf R, Klingel K, Bultmann B, Muller T, et al. Predictors of outcome in patients with suspected myocarditis. Circulation. 2008;118:639–48.PubMedCrossRef Kindermann I, Kindermann M, Kandolf R, Klingel K, Bultmann B, Muller T, et al. Predictors of outcome in patients with suspected myocarditis. Circulation. 2008;118:639–48.PubMedCrossRef
35.
go back to reference Berg KE, Ljungcrantz I, Andersson L, Bryngelsson C, Hedblad B, Fredrikson GN, et al. Elevated CD14++ CD16- monocytes predict cardiovascular events. Circ Cardiovasc Genet. 2012;5:122–31.PubMedCrossRef Berg KE, Ljungcrantz I, Andersson L, Bryngelsson C, Hedblad B, Fredrikson GN, et al. Elevated CD14++ CD16- monocytes predict cardiovascular events. Circ Cardiovasc Genet. 2012;5:122–31.PubMedCrossRef
36.
go back to reference Emami H, Singh P, MacNabb M, Vucic E, Lavender Z, Rudd JHF, et al. Splenic metabolic activity predicts risk of future cardiovascular events demonstration of a cardiosplenic axis in humans. JACC: CARDIOVASCULAR IMAGING; 2015. Emami H, Singh P, MacNabb M, Vucic E, Lavender Z, Rudd JHF, et al. Splenic metabolic activity predicts risk of future cardiovascular events demonstration of a cardiosplenic axis in humans. JACC: CARDIOVASCULAR IMAGING; 2015.
37.
go back to reference Biasucci LM, Liuzzo G, Grillo RL, Caligiuri G, Rebuzzi AG, Buffon A, et al. Elevated levels of C-reactive protein at discharge in patients with unstable angina predict recurrent instability. Circulation. 1999;99:855–60.PubMedCrossRef Biasucci LM, Liuzzo G, Grillo RL, Caligiuri G, Rebuzzi AG, Buffon A, et al. Elevated levels of C-reactive protein at discharge in patients with unstable angina predict recurrent instability. Circulation. 1999;99:855–60.PubMedCrossRef
38.
go back to reference Torre-Amione G, Kapadia S, Benedict C, Oral H, Young JB, Mann DL. Proinflammatory cytokine levels in patients with depressed left ventricular ejection fraction: a report from the Studies of Left Ventricular Dysfunction (SOLVD). J Am Coll Cardiol. 1996;27:1201–6.PubMedCrossRef Torre-Amione G, Kapadia S, Benedict C, Oral H, Young JB, Mann DL. Proinflammatory cytokine levels in patients with depressed left ventricular ejection fraction: a report from the Studies of Left Ventricular Dysfunction (SOLVD). J Am Coll Cardiol. 1996;27:1201–6.PubMedCrossRef
39.
go back to reference Deswal A, Petersen NJ, Feldman AM, Young JB, White BG, Mann DL. Cytokines and cytokine receptors in advanced heart failure: an analysis of the cytokine database from the Vesnarinone trial (VEST). Circulation. 2001;103:2055–9.PubMedCrossRef Deswal A, Petersen NJ, Feldman AM, Young JB, White BG, Mann DL. Cytokines and cytokine receptors in advanced heart failure: an analysis of the cytokine database from the Vesnarinone trial (VEST). Circulation. 2001;103:2055–9.PubMedCrossRef
40.
go back to reference Savvatis K, Pappritz K, Becher PM, Lindner D, Zietsch C, Volk HD, et al. Interleukin-23 deficiency leads to impaired wound healing and adverse prognosis after myocardial infarction. Circ Heart Fail. 2014;7:161–71.PubMedCrossRef Savvatis K, Pappritz K, Becher PM, Lindner D, Zietsch C, Volk HD, et al. Interleukin-23 deficiency leads to impaired wound healing and adverse prognosis after myocardial infarction. Circ Heart Fail. 2014;7:161–71.PubMedCrossRef
41.
go back to reference Riad A, Jager S, Sobirey M, Escher F, Yaulema-Riss A, Westermann D, et al. Toll-like receptor-4 modulates survival by induction of left ventricular remodeling after myocardial infarction in mice. J Immunol. 2008;180:6954–61.PubMedCrossRef Riad A, Jager S, Sobirey M, Escher F, Yaulema-Riss A, Westermann D, et al. Toll-like receptor-4 modulates survival by induction of left ventricular remodeling after myocardial infarction in mice. J Immunol. 2008;180:6954–61.PubMedCrossRef
42.
go back to reference Riad A, Westermann D, Zietsch C, Savvatis K, Becher PM, Bereswill S, et al. TRIF is a critical survival factor in viral cardiomyopathy. J Immunol. 2011;186:2561–70.PubMedCrossRef Riad A, Westermann D, Zietsch C, Savvatis K, Becher PM, Bereswill S, et al. TRIF is a critical survival factor in viral cardiomyopathy. J Immunol. 2011;186:2561–70.PubMedCrossRef
43.
go back to reference Kubota T, McTiernan CF, Frye CS, Slawson SE, Lemster BH, Koretsky AP, et al. Dilated cardiomyopathy in transgenic mice with cardiac-specific overexpression of tumor necrosis factor-alpha. Circ Res. 1997;81:627–35.PubMedCrossRef Kubota T, McTiernan CF, Frye CS, Slawson SE, Lemster BH, Koretsky AP, et al. Dilated cardiomyopathy in transgenic mice with cardiac-specific overexpression of tumor necrosis factor-alpha. Circ Res. 1997;81:627–35.PubMedCrossRef
44.
go back to reference Westermann D, Van Linthout S, Dhayat S, Dhayat N, Schmidt A, Noutsias M, et al. Tumor necrosis factor-alpha antagonism protects from myocardial inflammation and fibrosis in experimental diabetic cardiomyopathy. Basic Res Cardiol. 2007;102:500–7.PubMedCrossRef Westermann D, Van Linthout S, Dhayat S, Dhayat N, Schmidt A, Noutsias M, et al. Tumor necrosis factor-alpha antagonism protects from myocardial inflammation and fibrosis in experimental diabetic cardiomyopathy. Basic Res Cardiol. 2007;102:500–7.PubMedCrossRef
45.
go back to reference Savvatis K, Muller I, Frohlich M, Pappritz K, Zietsch C, Hamdani N, et al. Interleukin-6 receptor inhibition modulates the immune reaction and restores titin phosphorylation in experimental myocarditis. Basic Res Cardiol. 2014;109:449.PubMedCrossRef Savvatis K, Muller I, Frohlich M, Pappritz K, Zietsch C, Hamdani N, et al. Interleukin-6 receptor inhibition modulates the immune reaction and restores titin phosphorylation in experimental myocarditis. Basic Res Cardiol. 2014;109:449.PubMedCrossRef
46.
go back to reference Westermann D, Van Linthout S, Dhayat S, Dhayat N, Escher F, Bucker-Gartner C, et al. Cardioprotective and anti-inflammatory effects of interleukin converting enzyme inhibition in experimental diabetic cardiomyopathy. Diabetes. 2007;56:1834–41.PubMedCrossRef Westermann D, Van Linthout S, Dhayat S, Dhayat N, Escher F, Bucker-Gartner C, et al. Cardioprotective and anti-inflammatory effects of interleukin converting enzyme inhibition in experimental diabetic cardiomyopathy. Diabetes. 2007;56:1834–41.PubMedCrossRef
47.
go back to reference Koch M, Savvatis K, Scheeler M, Dhayat S, Bonaventura K, Pohl T, et al. Immunosuppression with an interleukin-2 fusion protein leads to improved LV function in experimental ischemic cardiomyopathy. Int Immunopharmacol. 2010;10:207–12.PubMedCrossRef Koch M, Savvatis K, Scheeler M, Dhayat S, Bonaventura K, Pohl T, et al. Immunosuppression with an interleukin-2 fusion protein leads to improved LV function in experimental ischemic cardiomyopathy. Int Immunopharmacol. 2010;10:207–12.PubMedCrossRef
48.
go back to reference Leuschner F, Courties G, Dutta P, Mortensen LJ, Gorbatov R, Sena B, et al. Silencing of CCR2 in myocarditis. Eur Heart J. 2015;36:1478–88.PubMedCrossRef Leuschner F, Courties G, Dutta P, Mortensen LJ, Gorbatov R, Sena B, et al. Silencing of CCR2 in myocarditis. Eur Heart J. 2015;36:1478–88.PubMedCrossRef
49.
go back to reference Van Linthout S, Riad A, Dhayat N, Spillmann F, Du J, Dhayat S, et al. Anti-inflammatory effects of atorvastatin improve left ventricular function in experimental diabetic cardiomyopathy. Diabetologia. 2007;50:1977–86.PubMedCrossRef Van Linthout S, Riad A, Dhayat N, Spillmann F, Du J, Dhayat S, et al. Anti-inflammatory effects of atorvastatin improve left ventricular function in experimental diabetic cardiomyopathy. Diabetologia. 2007;50:1977–86.PubMedCrossRef
50.
go back to reference Van Linthout S, Spillmann F, Riad A, Trimpert C, Lievens J, Meloni M, et al. Human apolipoprotein AI gene transfer reduces the development of experimental diabetic cardiomyopathy. Circulation. 2008;117:1563–73.PubMedCrossRef Van Linthout S, Spillmann F, Riad A, Trimpert C, Lievens J, Meloni M, et al. Human apolipoprotein AI gene transfer reduces the development of experimental diabetic cardiomyopathy. Circulation. 2008;117:1563–73.PubMedCrossRef
51.
go back to reference Van Linthout S, Spillmann F, Graiani G, Miteva K, Peng J, Van Craeyveld E, et al. Down-regulation of endothelial TLR4 signalling after apo AI gene transfer contributes to improved survival in an experimental model of lipopolysaccharide-induced inflammation. J Mol Med (Berl). 2011;89:151–60.CrossRef Van Linthout S, Spillmann F, Graiani G, Miteva K, Peng J, Van Craeyveld E, et al. Down-regulation of endothelial TLR4 signalling after apo AI gene transfer contributes to improved survival in an experimental model of lipopolysaccharide-induced inflammation. J Mol Med (Berl). 2011;89:151–60.CrossRef
52.
go back to reference Van Linthout S, Savvatis K, Miteva K, Peng J, Ringe J, Warstat K, et al. Mesenchymal stem cells improve murine acute coxsackievirus B3-induced myocarditis. Eur Heart J. 2011;32:2168–78.PubMedCrossRef Van Linthout S, Savvatis K, Miteva K, Peng J, Ringe J, Warstat K, et al. Mesenchymal stem cells improve murine acute coxsackievirus B3-induced myocarditis. Eur Heart J. 2011;32:2168–78.PubMedCrossRef
53.
go back to reference Savvatis K, van Linthout S, Miteva K, Pappritz K, Westermann D, Schefold JC, et al. Mesenchymal stromal cells but not cardiac fibroblasts exert beneficial systemic immunomodulatory effects in experimental myocarditis. PLoS One. 2012;7:e41047.PubMedPubMedCentralCrossRef Savvatis K, van Linthout S, Miteva K, Pappritz K, Westermann D, Schefold JC, et al. Mesenchymal stromal cells but not cardiac fibroblasts exert beneficial systemic immunomodulatory effects in experimental myocarditis. PLoS One. 2012;7:e41047.PubMedPubMedCentralCrossRef
54.
go back to reference K. Miteva, K. Pappritz, M. El-Shafeey, F. Dong, J. Ringe, C. Tschope, S. Van Linthout, Mesenchymal stromal cells modulate monocytes trafficking in Coxsackievirus B3-induced myocarditis, Stem Cells Transl Med, 2017. K. Miteva, K. Pappritz, M. El-Shafeey, F. Dong, J. Ringe, C. Tschope, S. Van Linthout, Mesenchymal stromal cells modulate monocytes trafficking in Coxsackievirus B3-induced myocarditis, Stem Cells Transl Med, 2017.
55.
go back to reference Miteva K, Haag M, Peng J, Savvatis K, Becher PM, Seifert M, et al. Human cardiac-derived adherent proliferating cells reduce murine acute Coxsackievirus B3-induced myocarditis. PLoS One. 2011;6:e28513.PubMedPubMedCentralCrossRef Miteva K, Haag M, Peng J, Savvatis K, Becher PM, Seifert M, et al. Human cardiac-derived adherent proliferating cells reduce murine acute Coxsackievirus B3-induced myocarditis. PLoS One. 2011;6:e28513.PubMedPubMedCentralCrossRef
56.
go back to reference Miteva K, Van Linthout S, Pappritz K, Muller I, Spillmann F, Haag M, et al. Human endomyocardial biopsy specimen-derived stromal cells modulate angiotensin II-induced cardiac remodeling. Stem Cells Transl Med. 2016;5:1707–18.PubMedCrossRef Miteva K, Van Linthout S, Pappritz K, Muller I, Spillmann F, Haag M, et al. Human endomyocardial biopsy specimen-derived stromal cells modulate angiotensin II-induced cardiac remodeling. Stem Cells Transl Med. 2016;5:1707–18.PubMedCrossRef
57.
go back to reference Wu CK, Lee JK, Chiang FT, Yang CH, Huang SW, Hwang JJ, et al. Plasma levels of tumor necrosis factor-alpha and interleukin-6 are associated with diastolic heart failure through downregulation of sarcoplasmic reticulum Ca2+ ATPase. Crit Care Med. 2011;39:984–92.PubMedCrossRef Wu CK, Lee JK, Chiang FT, Yang CH, Huang SW, Hwang JJ, et al. Plasma levels of tumor necrosis factor-alpha and interleukin-6 are associated with diastolic heart failure through downregulation of sarcoplasmic reticulum Ca2+ ATPase. Crit Care Med. 2011;39:984–92.PubMedCrossRef
58.
go back to reference Thaik CM, Calderone A, Takahashi N, Colucci WS. Interleukin-1 beta modulates the growth and phenotype of neonatal rat cardiac myocytes. J Clin Invest. 1995;96:1093–9.PubMedPubMedCentralCrossRef Thaik CM, Calderone A, Takahashi N, Colucci WS. Interleukin-1 beta modulates the growth and phenotype of neonatal rat cardiac myocytes. J Clin Invest. 1995;96:1093–9.PubMedPubMedCentralCrossRef
59.
go back to reference Yokoyama T, Vaca L, Rossen RD, Durante W, Hazarika P, Mann DL. Cellular basis for the negative inotropic effects of tumor necrosis factor-alpha in the adult mammalian heart. J Clin Invest. 1993;92:2303–12.PubMedPubMedCentralCrossRef Yokoyama T, Vaca L, Rossen RD, Durante W, Hazarika P, Mann DL. Cellular basis for the negative inotropic effects of tumor necrosis factor-alpha in the adult mammalian heart. J Clin Invest. 1993;92:2303–12.PubMedPubMedCentralCrossRef
60.
go back to reference Sedej S, Schmidt A, Denegri M, Walther S, Matovina M, Arnstein G, et al. Subclinical abnormalities in sarcoplasmic reticulum Ca(2+) release promote eccentric myocardial remodeling and pump failure death in response to pressure overload. J Am Coll Cardiol. 2014;63:1569–79.PubMedCrossRef Sedej S, Schmidt A, Denegri M, Walther S, Matovina M, Arnstein G, et al. Subclinical abnormalities in sarcoplasmic reticulum Ca(2+) release promote eccentric myocardial remodeling and pump failure death in response to pressure overload. J Am Coll Cardiol. 2014;63:1569–79.PubMedCrossRef
61.
go back to reference Tschope C, Lam CS. Diastolic heart failure: what we still don’t know. Looking for new concepts, diagnostic approaches, and the role of comorbidities. Herz. 2012;37:875–9.PubMedCrossRef Tschope C, Lam CS. Diastolic heart failure: what we still don’t know. Looking for new concepts, diagnostic approaches, and the role of comorbidities. Herz. 2012;37:875–9.PubMedCrossRef
62.
go back to reference Yokoyama T, Nakano M, Bednarczyk JL, McIntyre BW, Entman M, Mann DL. Tumor necrosis factor-alpha provokes a hypertrophic growth response in adult cardiac myocytes. Circulation. 1997;95:1247–52.PubMedCrossRef Yokoyama T, Nakano M, Bednarczyk JL, McIntyre BW, Entman M, Mann DL. Tumor necrosis factor-alpha provokes a hypertrophic growth response in adult cardiac myocytes. Circulation. 1997;95:1247–52.PubMedCrossRef
63.
go back to reference Condorelli G, Morisco C, Latronico MV, Claudio PP, Dent P, Tsichlis P, et al. TNF-alpha signal transduction in rat neonatal cardiac myocytes: definition of pathways generating from the TNF-alpha receptor. FASEB J. 2002;16:1732–7.PubMedCrossRef Condorelli G, Morisco C, Latronico MV, Claudio PP, Dent P, Tsichlis P, et al. TNF-alpha signal transduction in rat neonatal cardiac myocytes: definition of pathways generating from the TNF-alpha receptor. FASEB J. 2002;16:1732–7.PubMedCrossRef
64.
go back to reference Takahashi M. NLRP3 inflammasome as a novel player in myocardial infarction. Int Heart J. 2014;55:101–5.PubMedCrossRef Takahashi M. NLRP3 inflammasome as a novel player in myocardial infarction. Int Heart J. 2014;55:101–5.PubMedCrossRef
65.
go back to reference Gurantz D, Cowling RT, Varki N, Frikovsky E, Moore CD, Greenberg BH. IL-1beta and TNF-alpha upregulate angiotensin II type 1 (AT1) receptors on cardiac fibroblasts and are associated with increased AT1 density in the post-MI heart. J Mol Cell Cardiol. 2005;38:505–15.PubMedCrossRef Gurantz D, Cowling RT, Varki N, Frikovsky E, Moore CD, Greenberg BH. IL-1beta and TNF-alpha upregulate angiotensin II type 1 (AT1) receptors on cardiac fibroblasts and are associated with increased AT1 density in the post-MI heart. J Mol Cell Cardiol. 2005;38:505–15.PubMedCrossRef
66.
go back to reference Peng J, Gurantz D, Tran V, Cowling RT, Greenberg BH. Tumor necrosis factor-alpha-induced AT1 receptor upregulation enhances angiotensin II-mediated cardiac fibroblast responses that favor fibrosis. Circ Res. 2002;91:1119–26.PubMedCrossRef Peng J, Gurantz D, Tran V, Cowling RT, Greenberg BH. Tumor necrosis factor-alpha-induced AT1 receptor upregulation enhances angiotensin II-mediated cardiac fibroblast responses that favor fibrosis. Circ Res. 2002;91:1119–26.PubMedCrossRef
67.
go back to reference Wang Y, Li Y, Wu Y, Jia L, Wang J, Xie B, et al. 5TNF-alpha and IL-1beta neutralization ameliorates angiotensin II-induced cardiac damage in male mice. Endocrinology. 2014;155:2677–87.PubMedCrossRef Wang Y, Li Y, Wu Y, Jia L, Wang J, Xie B, et al. 5TNF-alpha and IL-1beta neutralization ameliorates angiotensin II-induced cardiac damage in male mice. Endocrinology. 2014;155:2677–87.PubMedCrossRef
68.
go back to reference Sullivan DE, Ferris M, Nguyen H, Abboud E, Brody AR. TNF-alpha induces TGF-beta1 expression in lung fibroblasts at the transcriptional level via AP-1 activation. J Cell Mol Med. 2009;13:1866–76.PubMedPubMedCentralCrossRef Sullivan DE, Ferris M, Nguyen H, Abboud E, Brody AR. TNF-alpha induces TGF-beta1 expression in lung fibroblasts at the transcriptional level via AP-1 activation. J Cell Mol Med. 2009;13:1866–76.PubMedPubMedCentralCrossRef
69.
go back to reference Voloshenyuk TG, Hart AD, Khoutorova E, Gardner JD. TNF-alpha increases cardiac fibroblast lysyl oxidase expression through TGF-beta and PI3Kinase signaling pathways. Biochem Biophys Res Commun. 2011;413:370–5.PubMedCrossRef Voloshenyuk TG, Hart AD, Khoutorova E, Gardner JD. TNF-alpha increases cardiac fibroblast lysyl oxidase expression through TGF-beta and PI3Kinase signaling pathways. Biochem Biophys Res Commun. 2011;413:370–5.PubMedCrossRef
70.
go back to reference Yokoyama C, Aoyama T, Ido T, Kakino A, Shiraki T, Tanaka T, et al. Deletion of LOX-1 protects against heart failure induced by doxorubicin. PLoS One. 2016;11:e0154994.PubMedPubMedCentralCrossRef Yokoyama C, Aoyama T, Ido T, Kakino A, Shiraki T, Tanaka T, et al. Deletion of LOX-1 protects against heart failure induced by doxorubicin. PLoS One. 2016;11:e0154994.PubMedPubMedCentralCrossRef
71.
go back to reference Yang J, Savvatis K, Kang JS, Fan P, Zhong H, Schwartz K, et al. Targeting LOXL2 for cardiac interstitial fibrosis and heart failure treatment. Nat Commun. 2016;7:13710.PubMedPubMedCentralCrossRef Yang J, Savvatis K, Kang JS, Fan P, Zhong H, Schwartz K, et al. Targeting LOXL2 for cardiac interstitial fibrosis and heart failure treatment. Nat Commun. 2016;7:13710.PubMedPubMedCentralCrossRef
72.
go back to reference C. Humeres, R. Vivar, P. Boza, C. Munoz, S. Bolivar, R. Anfossi, J.M. Osorio, F. Olivares-Silva, L. Garcia, G. Diaz-Araya, Cardiac fibroblast cytokine profiles induced by proinflammatory or profibrotic stimuli promote monocyte recruitment and modulate macrophage M1/M2 balance in vitro, J Mol Cell Cardiol, 2016. C. Humeres, R. Vivar, P. Boza, C. Munoz, S. Bolivar, R. Anfossi, J.M. Osorio, F. Olivares-Silva, L. Garcia, G. Diaz-Araya, Cardiac fibroblast cytokine profiles induced by proinflammatory or profibrotic stimuli promote monocyte recruitment and modulate macrophage M1/M2 balance in vitro, J Mol Cell Cardiol, 2016.
73.
go back to reference Tschope C, Van Linthout S. New insights in (inter)cellular mechanisms by heart failure with preserved ejection fraction. Curr Heart Fail Rep. 2014;11:436–44.PubMedPubMedCentralCrossRef Tschope C, Van Linthout S. New insights in (inter)cellular mechanisms by heart failure with preserved ejection fraction. Curr Heart Fail Rep. 2014;11:436–44.PubMedPubMedCentralCrossRef
74.
go back to reference Bang C, Antoniades C, Antonopoulos AS, Eriksson U, Franssen C, Hamdani N, et al. Intercellular communication lessons in heart failure. Eur J Heart Fail. 2015;17:1091–103.PubMedCrossRef Bang C, Antoniades C, Antonopoulos AS, Eriksson U, Franssen C, Hamdani N, et al. Intercellular communication lessons in heart failure. Eur J Heart Fail. 2015;17:1091–103.PubMedCrossRef
75.
go back to reference Tamaru M, Tomura K, Sakamoto S, Tezuka K, Tamatani T, Narumi S. Interleukin-1beta induces tissue- and cell type-specific expression of adhesion molecules in vivo. Arterioscler Thromb Vasc Biol. 1998;18:1292–303.PubMedCrossRef Tamaru M, Tomura K, Sakamoto S, Tezuka K, Tamatani T, Narumi S. Interleukin-1beta induces tissue- and cell type-specific expression of adhesion molecules in vivo. Arterioscler Thromb Vasc Biol. 1998;18:1292–303.PubMedCrossRef
76.
go back to reference Zakrzewicz A, Grafe M, Terbeek D, Bongrazio M, Auch-Schwelk W, Walzog B, et al. L-selectin-dependent leukocyte adhesion to microvascular but not to macrovascular endothelial cells of the human coronary system. Blood. 1997;89:3228–35.PubMed Zakrzewicz A, Grafe M, Terbeek D, Bongrazio M, Auch-Schwelk W, Walzog B, et al. L-selectin-dependent leukocyte adhesion to microvascular but not to macrovascular endothelial cells of the human coronary system. Blood. 1997;89:3228–35.PubMed
77.
go back to reference Woodfin A, Voisin MB, Imhof BA, Dejana E, Engelhardt B, Nourshargh S. Endothelial cell activation leads to neutrophil transmigration as supported by the sequential roles of ICAM-2, JAM-A, and PECAM-1. Blood. 2009;113:6246–57.PubMedPubMedCentralCrossRef Woodfin A, Voisin MB, Imhof BA, Dejana E, Engelhardt B, Nourshargh S. Endothelial cell activation leads to neutrophil transmigration as supported by the sequential roles of ICAM-2, JAM-A, and PECAM-1. Blood. 2009;113:6246–57.PubMedPubMedCentralCrossRef
78.
go back to reference Chandrasekar B, Vemula K, Surabhi RM, Li-Weber M, Owen-Schaub LB, Jensen LE, et al. Activation of intrinsic and extrinsic proapoptotic signaling pathways in interleukin-18-mediated human cardiac endothelial cell death. J Biol Chem. 2004;279:20221–33.PubMedCrossRef Chandrasekar B, Vemula K, Surabhi RM, Li-Weber M, Owen-Schaub LB, Jensen LE, et al. Activation of intrinsic and extrinsic proapoptotic signaling pathways in interleukin-18-mediated human cardiac endothelial cell death. J Biol Chem. 2004;279:20221–33.PubMedCrossRef
79.
go back to reference Okada H, Woodcock-Mitchell J, Mitchell J, Sakamoto T, Marutsuka K, Sobel BE, et al. Induction of plasminogen activator inhibitor type 1 and type 1 collagen expression in rat cardiac microvascular endothelial cells by interleukin-1 and its dependence on oxygen-centered free radicals. Circulation. 1998;97:2175–82.PubMedCrossRef Okada H, Woodcock-Mitchell J, Mitchell J, Sakamoto T, Marutsuka K, Sobel BE, et al. Induction of plasminogen activator inhibitor type 1 and type 1 collagen expression in rat cardiac microvascular endothelial cells by interleukin-1 and its dependence on oxygen-centered free radicals. Circulation. 1998;97:2175–82.PubMedCrossRef
80.
go back to reference Zeisberg EM, Tarnavski O, Zeisberg M, Dorfman AL, McMullen JR, Gustafsson E, et al. Endothelial-to-mesenchymal transition contributes to cardiac fibrosis. Nat Med. 2007;13:952–61.PubMedCrossRef Zeisberg EM, Tarnavski O, Zeisberg M, Dorfman AL, McMullen JR, Gustafsson E, et al. Endothelial-to-mesenchymal transition contributes to cardiac fibrosis. Nat Med. 2007;13:952–61.PubMedCrossRef
81.
go back to reference Chen W, Spitzl A, Mathes D, Nikolaev VO, Werner F, Weirather J, et al. Endothelial actions of ANP enhance myocardial inflammatory infiltration in the early phase after acute infarction. Circ Res. 2016;119:237–48.PubMedCrossRef Chen W, Spitzl A, Mathes D, Nikolaev VO, Werner F, Weirather J, et al. Endothelial actions of ANP enhance myocardial inflammatory infiltration in the early phase after acute infarction. Circ Res. 2016;119:237–48.PubMedCrossRef
82.
go back to reference Hu YF, Chen YJ, Lin YJ, Chen SA. Inflammation and the pathogenesis of atrial fibrillation. Nat Rev Cardiol. 2015;12:230–43.PubMedCrossRef Hu YF, Chen YJ, Lin YJ, Chen SA. Inflammation and the pathogenesis of atrial fibrillation. Nat Rev Cardiol. 2015;12:230–43.PubMedCrossRef
83.
go back to reference Shimano M, Ouchi N, Walsh K. Cardiokines: recent progress in elucidating the cardiac secretome. Circulation. 2012;126:e327–32.PubMedCrossRef Shimano M, Ouchi N, Walsh K. Cardiokines: recent progress in elucidating the cardiac secretome. Circulation. 2012;126:e327–32.PubMedCrossRef
84.
go back to reference Kapadia S, Lee J, Torre-Amione G, Birdsall HH, Ma TS, Mann DL. Tumor necrosis factor-alpha gene and protein expression in adult feline myocardium after endotoxin administration. J Clin Invest. 1995;96:1042–52.PubMedPubMedCentralCrossRef Kapadia S, Lee J, Torre-Amione G, Birdsall HH, Ma TS, Mann DL. Tumor necrosis factor-alpha gene and protein expression in adult feline myocardium after endotoxin administration. J Clin Invest. 1995;96:1042–52.PubMedPubMedCentralCrossRef
85.
go back to reference Liu Y, Lian K, Zhang L, Wang R, Yi F, Gao C, et al. TXNIP mediates NLRP3 inflammasome activation in cardiac microvascular endothelial cells as a novel mechanism in myocardial ischemia/reperfusion injury. Basic Res Cardiol. 2014;109:415.PubMedCrossRef Liu Y, Lian K, Zhang L, Wang R, Yi F, Gao C, et al. TXNIP mediates NLRP3 inflammasome activation in cardiac microvascular endothelial cells as a novel mechanism in myocardial ischemia/reperfusion injury. Basic Res Cardiol. 2014;109:415.PubMedCrossRef
86.
go back to reference Pinto AR, Ilinykh A, Ivey MJ, Kuwabara JT, D'Antoni ML, Debuque R, et al. Revisiting cardiac cellular composition. Circ Res. 2016;118:400–9.PubMedCrossRef Pinto AR, Ilinykh A, Ivey MJ, Kuwabara JT, D'Antoni ML, Debuque R, et al. Revisiting cardiac cellular composition. Circ Res. 2016;118:400–9.PubMedCrossRef
87.
go back to reference Torre-Amione G, Kapadia S, Lee J, Bies RD, Lebovitz R, Mann DL. Expression and functional significance of tumor necrosis factor receptors in human myocardium. Circulation. 1995;92:1487–93.PubMedCrossRef Torre-Amione G, Kapadia S, Lee J, Bies RD, Lebovitz R, Mann DL. Expression and functional significance of tumor necrosis factor receptors in human myocardium. Circulation. 1995;92:1487–93.PubMedCrossRef
88.
go back to reference Toldo S, Kannan H, Bussani R, Anzini M, Sonnino C, Sinagra G, et al. Formation of the inflammasome in acute myocarditis. Int J Cardiol. 2014;171:e119–21.PubMedCrossRef Toldo S, Kannan H, Bussani R, Anzini M, Sonnino C, Sinagra G, et al. Formation of the inflammasome in acute myocarditis. Int J Cardiol. 2014;171:e119–21.PubMedCrossRef
89.
go back to reference Sager HB, Hulsmans M, Lavine KJ, Moreira MB, Heidt T, Courties G, et al. Proliferation and recruitment contribute to myocardial macrophage expansion in chronic heart failure. Circ Res. 2016;119:853–64.PubMedCrossRef Sager HB, Hulsmans M, Lavine KJ, Moreira MB, Heidt T, Courties G, et al. Proliferation and recruitment contribute to myocardial macrophage expansion in chronic heart failure. Circ Res. 2016;119:853–64.PubMedCrossRef
92.
go back to reference Courties G, Heidt T, Sebas M, Iwamoto Y, Jeon D, Truelove J, et al. In vivo silencing of the transcription factor IRF5 reprograms the macrophage phenotype and improves infarct healing. J Am Coll Cardiol. 2014;63:1556–66.PubMedCrossRef Courties G, Heidt T, Sebas M, Iwamoto Y, Jeon D, Truelove J, et al. In vivo silencing of the transcription factor IRF5 reprograms the macrophage phenotype and improves infarct healing. J Am Coll Cardiol. 2014;63:1556–66.PubMedCrossRef
93.
go back to reference Kim EJ, Kim S, Kang DO, Seo HS. Metabolic activity of the spleen and bone marrow in patients with acute myocardial infarction evaluated by 18f-fluorodeoxyglucose positron emission tomograpic imaging. Circ Cardiovasc Imaging. 2014;7:454–60.PubMedCrossRef Kim EJ, Kim S, Kang DO, Seo HS. Metabolic activity of the spleen and bone marrow in patients with acute myocardial infarction evaluated by 18f-fluorodeoxyglucose positron emission tomograpic imaging. Circ Cardiovasc Imaging. 2014;7:454–60.PubMedCrossRef
94.
95.
go back to reference Swirski FK, Nahrendorf M, Etzrodt M, Wildgruber M, Cortez-Retamozo V, Panizzi P, et al. Identification of splenic reservoir monocytes and their deployment to inflammatory sites. Science. 2009;325:612–6.PubMedPubMedCentralCrossRef Swirski FK, Nahrendorf M, Etzrodt M, Wildgruber M, Cortez-Retamozo V, Panizzi P, et al. Identification of splenic reservoir monocytes and their deployment to inflammatory sites. Science. 2009;325:612–6.PubMedPubMedCentralCrossRef
96.
go back to reference Ismahil MA, Hamid T, Bansal SS, Patel B, Kingery JR, Prabhu SD. Remodeling of the mononuclear phagocyte network underlies chronic inflammation and disease progression in heart failure: critical importance of the cardiosplenic axis. Circ Res. 2014;114:266–82.PubMedCrossRef Ismahil MA, Hamid T, Bansal SS, Patel B, Kingery JR, Prabhu SD. Remodeling of the mononuclear phagocyte network underlies chronic inflammation and disease progression in heart failure: critical importance of the cardiosplenic axis. Circ Res. 2014;114:266–82.PubMedCrossRef
97.
go back to reference Leuschner F, Panizzi P, Chico-Calero I, Lee WW, Ueno T, Cortez-Retamozo V, et al. Angiotensin-converting enzyme inhibition prevents the release of monocytes from their splenic reservoir in mice with myocardial infarction. Circ Res. 2010:1364–73. Leuschner F, Panizzi P, Chico-Calero I, Lee WW, Ueno T, Cortez-Retamozo V, et al. Angiotensin-converting enzyme inhibition prevents the release of monocytes from their splenic reservoir in mice with myocardial infarction. Circ Res. 2010:1364–73.
98.
go back to reference van der Laan AM, Ter Horst EN, Delewi R, Begieneman MP, Krijnen PA, Hirsch A, et al. Monocyte subset accumulation in the human heart following acute myocardial infarction and the role of the spleen as monocyte reservoir. Eur Heart J. 2014;35:376–85.PubMedCrossRef van der Laan AM, Ter Horst EN, Delewi R, Begieneman MP, Krijnen PA, Hirsch A, et al. Monocyte subset accumulation in the human heart following acute myocardial infarction and the role of the spleen as monocyte reservoir. Eur Heart J. 2014;35:376–85.PubMedCrossRef
99.
go back to reference Tsujioka H, Imanishi T, Ikejima H, Kuroi A, Takarada S, Tanimoto T, et al. Impact of heterogeneity of human peripheral blood monocyte subsets on myocardial salvage in patients with primary acute myocardial infarction. J Am Coll Cardiol. 2009;54:130–8.PubMedCrossRef Tsujioka H, Imanishi T, Ikejima H, Kuroi A, Takarada S, Tanimoto T, et al. Impact of heterogeneity of human peripheral blood monocyte subsets on myocardial salvage in patients with primary acute myocardial infarction. J Am Coll Cardiol. 2009;54:130–8.PubMedCrossRef
100.
go back to reference Klingenberg R, Luscher TF. Rheumatoid arthritis and coronary atherosclerosis: two cousins engaging in a dangerous liaison. Eur Heart J. 2015;36:3423–5.PubMedPubMedCentralCrossRef Klingenberg R, Luscher TF. Rheumatoid arthritis and coronary atherosclerosis: two cousins engaging in a dangerous liaison. Eur Heart J. 2015;36:3423–5.PubMedPubMedCentralCrossRef
101.
go back to reference Mason JC, Libby P. Cardiovascular disease in patients with chronic inflammation: mechanisms underlying premature cardiovascular events in rheumatologic conditions. Eur Heart J. 2015;36:482–489c.PubMedCrossRef Mason JC, Libby P. Cardiovascular disease in patients with chronic inflammation: mechanisms underlying premature cardiovascular events in rheumatologic conditions. Eur Heart J. 2015;36:482–489c.PubMedCrossRef
102.
go back to reference Elenkov IJ, Wilder RL, Chrousos GP, Vizi ES. The sympathetic nerve--an integrative interface between two supersystems: the brain and the immune system. Pharmacol Rev. 2000;52:595–638.PubMed Elenkov IJ, Wilder RL, Chrousos GP, Vizi ES. The sympathetic nerve--an integrative interface between two supersystems: the brain and the immune system. Pharmacol Rev. 2000;52:595–638.PubMed
103.
go back to reference Ahlehoff O, Gislason GH, Jorgensen CH, Lindhardsen J, Charlot M, Olesen JB, et al. Psoriasis and risk of atrial fibrillation and ischaemic stroke: a Danish Nationwide Cohort Study. Eur Heart J. 2012;33:2054–64.PubMedCrossRef Ahlehoff O, Gislason GH, Jorgensen CH, Lindhardsen J, Charlot M, Olesen JB, et al. Psoriasis and risk of atrial fibrillation and ischaemic stroke: a Danish Nationwide Cohort Study. Eur Heart J. 2012;33:2054–64.PubMedCrossRef
104.
go back to reference P.E. Lazzerini, P.L. Capecchi, F. Laghi-Pasini, Systemic inflammation and arrhythmic risk: lessons from rheumatoid arthritis, Eur Heart J. 2016. P.E. Lazzerini, P.L. Capecchi, F. Laghi-Pasini, Systemic inflammation and arrhythmic risk: lessons from rheumatoid arthritis, Eur Heart J. 2016.
105.
go back to reference Xu H, Barnes GT, Yang Q, Tan G, Yang D, Chou CJ, et al. Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance. J Clin Invest. 2003;112:1821–30.PubMedPubMedCentralCrossRef Xu H, Barnes GT, Yang Q, Tan G, Yang D, Chou CJ, et al. Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance. J Clin Invest. 2003;112:1821–30.PubMedPubMedCentralCrossRef
106.
go back to reference Castoldi A, Naffah de Souza C, Camara NO, Moraes-Vieira PM. The macrophage switch in obesity development. Front Immunol. 2015;6:637.PubMed Castoldi A, Naffah de Souza C, Camara NO, Moraes-Vieira PM. The macrophage switch in obesity development. Front Immunol. 2015;6:637.PubMed
107.
go back to reference Ohashi K, Kihara S, Ouchi N, Kumada M, Fujita K, Hiuge A, et al. Adiponectin replenishment ameliorates obesity-related hypertension. Hypertension. 2006;47:1108–16.PubMedCrossRef Ohashi K, Kihara S, Ouchi N, Kumada M, Fujita K, Hiuge A, et al. Adiponectin replenishment ameliorates obesity-related hypertension. Hypertension. 2006;47:1108–16.PubMedCrossRef
108.
go back to reference Shibata R, Ouchi N, Ito M, Kihara S, Shiojima I, Pimentel DR, et al. Adiponectin-mediated modulation of hypertrophic signals in the heart. Nat Med. 2004;10:1384–9.PubMedPubMedCentralCrossRef Shibata R, Ouchi N, Ito M, Kihara S, Shiojima I, Pimentel DR, et al. Adiponectin-mediated modulation of hypertrophic signals in the heart. Nat Med. 2004;10:1384–9.PubMedPubMedCentralCrossRef
109.
go back to reference Shibata R, Sato K, Pimentel DR, Takemura Y, Kihara S, Ohashi K, et al. Adiponectin protects against myocardial ischemia-reperfusion injury through AMPK- and COX-2-dependent mechanisms. Nat Med. 2005;11:1096–103.PubMedPubMedCentralCrossRef Shibata R, Sato K, Pimentel DR, Takemura Y, Kihara S, Ohashi K, et al. Adiponectin protects against myocardial ischemia-reperfusion injury through AMPK- and COX-2-dependent mechanisms. Nat Med. 2005;11:1096–103.PubMedPubMedCentralCrossRef
110.
go back to reference Shibata R, Izumiya Y, Sato K, Papanicolaou K, Kihara S, Colucci WS, et al. Adiponectin protects against the development of systolic dysfunction following myocardial infarction. J Mol Cell Cardiol. 2007;42:1065–74.PubMedPubMedCentralCrossRef Shibata R, Izumiya Y, Sato K, Papanicolaou K, Kihara S, Colucci WS, et al. Adiponectin protects against the development of systolic dysfunction following myocardial infarction. J Mol Cell Cardiol. 2007;42:1065–74.PubMedPubMedCentralCrossRef
111.
go back to reference Sam F, Duhaney TA, Sato K, Wilson RM, Ohashi K, Sono-Romanelli S, et al. Adiponectin deficiency, diastolic dysfunction, and diastolic heart failure. Endocrinology. 2010;151:322–31.PubMedCrossRef Sam F, Duhaney TA, Sato K, Wilson RM, Ohashi K, Sono-Romanelli S, et al. Adiponectin deficiency, diastolic dysfunction, and diastolic heart failure. Endocrinology. 2010;151:322–31.PubMedCrossRef
112.
go back to reference Tanaka K, Wilson RM, Essick EE, Duffen JL, Scherer PE, Ouchi N, et al. Effects of adiponectin on calcium-handling proteins in heart failure with preserved ejection fraction. Circ Heart Fail. 2014;7:976–85.PubMedPubMedCentralCrossRef Tanaka K, Wilson RM, Essick EE, Duffen JL, Scherer PE, Ouchi N, et al. Effects of adiponectin on calcium-handling proteins in heart failure with preserved ejection fraction. Circ Heart Fail. 2014;7:976–85.PubMedPubMedCentralCrossRef
113.
go back to reference Nagareddy PR, Murphy AJ, Stirzaker RA, Hu Y, Yu S, Miller RG, et al. Hyperglycemia promotes myelopoiesis and impairs the resolution of atherosclerosis. Cell Metab. 2013;17:695–708.PubMedPubMedCentralCrossRef Nagareddy PR, Murphy AJ, Stirzaker RA, Hu Y, Yu S, Miller RG, et al. Hyperglycemia promotes myelopoiesis and impairs the resolution of atherosclerosis. Cell Metab. 2013;17:695–708.PubMedPubMedCentralCrossRef
114.
go back to reference Nagareddy PR, Kraakman M, Masters SL, Stirzaker RA, Gorman DJ, Grant RW, et al. Adipose tissue macrophages promote myelopoiesis and monocytosis in obesity. Cell Metab. 2014;19:821–35.PubMedPubMedCentralCrossRef Nagareddy PR, Kraakman M, Masters SL, Stirzaker RA, Gorman DJ, Grant RW, et al. Adipose tissue macrophages promote myelopoiesis and monocytosis in obesity. Cell Metab. 2014;19:821–35.PubMedPubMedCentralCrossRef
115.
go back to reference Franssen C, Chen S, Unger A, Korkmaz HI, De Keulenaer GW, Tschope C, et al. Myocardial microvascular inflammatory endothelial activation in heart failure with preserved ejection fraction. JACC Heart Fail. 2016;4:312–24.PubMedCrossRef Franssen C, Chen S, Unger A, Korkmaz HI, De Keulenaer GW, Tschope C, et al. Myocardial microvascular inflammatory endothelial activation in heart failure with preserved ejection fraction. JACC Heart Fail. 2016;4:312–24.PubMedCrossRef
116.
go back to reference Hamdani N, Franssen C, Lourenco A, Falcao-Pires I, Fontoura D, Leite S, et al. Myocardial titin hypophosphorylation importantly contributes to heart failure with preserved ejection fraction in a rat metabolic risk model. Circ Heart Fail. 2013;6:1239–49.PubMedCrossRef Hamdani N, Franssen C, Lourenco A, Falcao-Pires I, Fontoura D, Leite S, et al. Myocardial titin hypophosphorylation importantly contributes to heart failure with preserved ejection fraction in a rat metabolic risk model. Circ Heart Fail. 2013;6:1239–49.PubMedCrossRef
117.
go back to reference Hamdani N, Paulus WJ. Myocardial titin and collagen in cardiac diastolic dysfunction: partners in crime. Circulation. 2013;128:5–8.PubMedCrossRef Hamdani N, Paulus WJ. Myocardial titin and collagen in cardiac diastolic dysfunction: partners in crime. Circulation. 2013;128:5–8.PubMedCrossRef
118.
go back to reference Kasner M, Westermann D, Lopez B, Gaub R, Escher F, Kuhl U, et al. Diastolic tissue Doppler indexes correlate with the degree of collagen expression and cross-linking in heart failure and normal ejection fraction. J Am Coll Cardiol. 2011;57:977–85.PubMedCrossRef Kasner M, Westermann D, Lopez B, Gaub R, Escher F, Kuhl U, et al. Diastolic tissue Doppler indexes correlate with the degree of collagen expression and cross-linking in heart failure and normal ejection fraction. J Am Coll Cardiol. 2011;57:977–85.PubMedCrossRef
119.
go back to reference Murdoch CE, Chaubey S, Zeng L, Yu B, Ivetic A, Walker SJ, et al. Endothelial NADPH oxidase-2 promotes interstitial cardiac fibrosis and diastolic dysfunction through proinflammatory effects and endothelial-mesenchymal transition. J Am Coll Cardiol. 2014;63:2734–41.PubMedCrossRef Murdoch CE, Chaubey S, Zeng L, Yu B, Ivetic A, Walker SJ, et al. Endothelial NADPH oxidase-2 promotes interstitial cardiac fibrosis and diastolic dysfunction through proinflammatory effects and endothelial-mesenchymal transition. J Am Coll Cardiol. 2014;63:2734–41.PubMedCrossRef
120.
go back to reference Ogawa K, Hirooka Y, Kishi T, Ide T, Sunagawa K. Partially silencing brain toll-like receptor 4 prevents in part left ventricular remodeling with sympathoinhibition in rats with myocardial infarction-induced heart failure. PLoS One. 2013;8:e69053.PubMedPubMedCentralCrossRef Ogawa K, Hirooka Y, Kishi T, Ide T, Sunagawa K. Partially silencing brain toll-like receptor 4 prevents in part left ventricular remodeling with sympathoinhibition in rats with myocardial infarction-induced heart failure. PLoS One. 2013;8:e69053.PubMedPubMedCentralCrossRef
121.
go back to reference Kishi T. Heart failure as a disruption of dynamic circulatory homeostasis mediated by the brain. Int Heart J. 2016;57:145–9.PubMedCrossRef Kishi T. Heart failure as a disruption of dynamic circulatory homeostasis mediated by the brain. Int Heart J. 2016;57:145–9.PubMedCrossRef
123.
go back to reference Loncar G, Fulster S, von Haehling S, Popovic V. Metabolism and the heart: an overview of muscle, fat, and bone metabolism in heart failure. Int J Cardiol. 2013;162:77–85.PubMedCrossRef Loncar G, Fulster S, von Haehling S, Popovic V. Metabolism and the heart: an overview of muscle, fat, and bone metabolism in heart failure. Int J Cardiol. 2013;162:77–85.PubMedCrossRef
125.
go back to reference Yoshida T, Friehs I, Mummidi S, del Nido PJ, Addulnour-Nakhoul S, Delafontaine P, et al. Pressure overload induces IL-18 and IL-18R expression, but markedly suppresses IL-18BP expression in a rabbit model. IL-18 potentiates TNF-alpha-induced cardiomyocyte death. J Mol Cell Cardiol. 2014;75:141–51.PubMedPubMedCentralCrossRef Yoshida T, Friehs I, Mummidi S, del Nido PJ, Addulnour-Nakhoul S, Delafontaine P, et al. Pressure overload induces IL-18 and IL-18R expression, but markedly suppresses IL-18BP expression in a rabbit model. IL-18 potentiates TNF-alpha-induced cardiomyocyte death. J Mol Cell Cardiol. 2014;75:141–51.PubMedPubMedCentralCrossRef
126.
go back to reference Shyu KG, Wang BW, Lin CM, Chang H. Cyclic stretch enhances the expression of toll-like receptor 4 gene in cultured cardiomyocytes via p38 MAP kinase and NF-kappaB pathway. J Biomed Sci. 2010;17:15.PubMedPubMedCentralCrossRef Shyu KG, Wang BW, Lin CM, Chang H. Cyclic stretch enhances the expression of toll-like receptor 4 gene in cultured cardiomyocytes via p38 MAP kinase and NF-kappaB pathway. J Biomed Sci. 2010;17:15.PubMedPubMedCentralCrossRef
127.
go back to reference Honsho S, Nishikawa S, Amano K, Zen K, Adachi Y, Kishita E, et al. Pressure-mediated hypertrophy and mechanical stretch induces IL-1 release and subsequent IGF-1 generation to maintain compensative hypertrophy by affecting Akt and JNK pathways. Circ Res. 2009;105:1149–58.PubMedCrossRef Honsho S, Nishikawa S, Amano K, Zen K, Adachi Y, Kishita E, et al. Pressure-mediated hypertrophy and mechanical stretch induces IL-1 release and subsequent IGF-1 generation to maintain compensative hypertrophy by affecting Akt and JNK pathways. Circ Res. 2009;105:1149–58.PubMedCrossRef
128.
go back to reference Sager HB, Heidt T, Hulsmans M, Dutta P, Courties G, Sebas M, et al. Targeting interleukin-1beta reduces leukocyte production after acute myocardial infarction. Circulation. 2015;132:1880–90.PubMedPubMedCentral Sager HB, Heidt T, Hulsmans M, Dutta P, Courties G, Sebas M, et al. Targeting interleukin-1beta reduces leukocyte production after acute myocardial infarction. Circulation. 2015;132:1880–90.PubMedPubMedCentral
129.
go back to reference Davies PF. Hemodynamic shear stress and the endothelium in cardiovascular pathophysiology. Nat Clin Pract Cardiovasc Med. 2009;6:16–26.PubMedCrossRef Davies PF. Hemodynamic shear stress and the endothelium in cardiovascular pathophysiology. Nat Clin Pract Cardiovasc Med. 2009;6:16–26.PubMedCrossRef
130.
go back to reference McCormick ME, Manduchi E, Witschey WR, Gorman RC, Gorman JH 3rd, Jiang YZ, et al. Spatial phenotyping of the endocardial endothelium as a function of intracardiac hemodynamic shear stress. J Biomech. 2017;50:11–9.PubMedCrossRef McCormick ME, Manduchi E, Witschey WR, Gorman RC, Gorman JH 3rd, Jiang YZ, et al. Spatial phenotyping of the endocardial endothelium as a function of intracardiac hemodynamic shear stress. J Biomech. 2017;50:11–9.PubMedCrossRef
131.
go back to reference Pugin J, Dunn I, Jolliet P, Tassaux D, Magnenat JL, Nicod LP, et al. Activation of human macrophages by mechanical ventilation in vitro. Am J Phys. 1998;275:L1040–50. Pugin J, Dunn I, Jolliet P, Tassaux D, Magnenat JL, Nicod LP, et al. Activation of human macrophages by mechanical ventilation in vitro. Am J Phys. 1998;275:L1040–50.
132.
go back to reference Sakamoto H, Aikawa M, Hill CC, Weiss D, Taylor WR, Libby P, et al. Biomechanical strain induces class a scavenger receptor expression in human monocyte/macrophages and THP-1 cells: a potential mechanism of increased atherosclerosis in hypertension. Circulation. 2001;104:109–14.PubMedCrossRef Sakamoto H, Aikawa M, Hill CC, Weiss D, Taylor WR, Libby P, et al. Biomechanical strain induces class a scavenger receptor expression in human monocyte/macrophages and THP-1 cells: a potential mechanism of increased atherosclerosis in hypertension. Circulation. 2001;104:109–14.PubMedCrossRef
133.
go back to reference Boyd JH, Mathur S, Wang Y, Bateman RM, Walley KR. Toll-like receptor stimulation in cardiomyoctes decreases contractility and initiates an NF-kappaB dependent inflammatory response. Cardiovasc Res. 2006;72:384–93.PubMedCrossRef Boyd JH, Mathur S, Wang Y, Bateman RM, Walley KR. Toll-like receptor stimulation in cardiomyoctes decreases contractility and initiates an NF-kappaB dependent inflammatory response. Cardiovasc Res. 2006;72:384–93.PubMedCrossRef
134.
go back to reference Bliksoen M, Mariero LH, Torp MK, Baysa A, Ytrehus K, Haugen F, et al. Extracellular mtDNA activates NF-kappaB via toll-like receptor 9 and induces cell death in cardiomyocytes. Basic Res Cardiol. 2016;111:42.PubMedCrossRef Bliksoen M, Mariero LH, Torp MK, Baysa A, Ytrehus K, Haugen F, et al. Extracellular mtDNA activates NF-kappaB via toll-like receptor 9 and induces cell death in cardiomyocytes. Basic Res Cardiol. 2016;111:42.PubMedCrossRef
135.
go back to reference Tian J, Guo X, Liu XM, Liu L, Weng QF, Dong SJ, et al. Extracellular HSP60 induces inflammation through activating and up-regulating TLRs in cardiomyocytes. Cardiovasc Res. 2013;98:391–401.PubMedCrossRef Tian J, Guo X, Liu XM, Liu L, Weng QF, Dong SJ, et al. Extracellular HSP60 induces inflammation through activating and up-regulating TLRs in cardiomyocytes. Cardiovasc Res. 2013;98:391–401.PubMedCrossRef
136.
go back to reference Rohde D, Schon C, Boerries M, Didrihsone I, Ritterhoff J, Kubatzky KF, et al. S100A1 is released from ischemic cardiomyocytes and signals myocardial damage via toll-like receptor 4. EMBO Mol Med. 2014;6:778–94.PubMedPubMedCentralCrossRef Rohde D, Schon C, Boerries M, Didrihsone I, Ritterhoff J, Kubatzky KF, et al. S100A1 is released from ischemic cardiomyocytes and signals myocardial damage via toll-like receptor 4. EMBO Mol Med. 2014;6:778–94.PubMedPubMedCentralCrossRef
137.
go back to reference Volz HC, Laohachewin D, Seidel C, Lasitschka F, Keilbach K, Wienbrandt AR, et al. S100A8/A9 aggravates post-ischemic heart failure through activation of RAGE-dependent NF-kappaB signaling. Basic Res Cardiol. 2012;107:250.PubMedCrossRef Volz HC, Laohachewin D, Seidel C, Lasitschka F, Keilbach K, Wienbrandt AR, et al. S100A8/A9 aggravates post-ischemic heart failure through activation of RAGE-dependent NF-kappaB signaling. Basic Res Cardiol. 2012;107:250.PubMedCrossRef
138.
go back to reference Feng Y, Zhao H, Xu X, Buys ES, Raher MJ, Bopassa JC, et al. Innate immune adaptor MyD88 mediates neutrophil recruitment and myocardial injury after ischemia-reperfusion in mice. Am J Physiol Heart Circ Physiol. 2008;295:H1311–8.PubMedPubMedCentralCrossRef Feng Y, Zhao H, Xu X, Buys ES, Raher MJ, Bopassa JC, et al. Innate immune adaptor MyD88 mediates neutrophil recruitment and myocardial injury after ischemia-reperfusion in mice. Am J Physiol Heart Circ Physiol. 2008;295:H1311–8.PubMedPubMedCentralCrossRef
139.
go back to reference Midwood K, Sacre S, Piccinini AM, Inglis J, Trebaul A, Chan E, et al. Tenascin-C is an endogenous activator of toll-like receptor 4 that is essential for maintaining inflammation in arthritic joint disease. Nat Med. 2009;15:774–80.PubMedCrossRef Midwood K, Sacre S, Piccinini AM, Inglis J, Trebaul A, Chan E, et al. Tenascin-C is an endogenous activator of toll-like receptor 4 that is essential for maintaining inflammation in arthritic joint disease. Nat Med. 2009;15:774–80.PubMedCrossRef
140.
go back to reference Nishioka T, Onishi K, Shimojo N, Nagano Y, Matsusaka H, Ikeuchi M, et al. Tenascin-C may aggravate left ventricular remodeling and function after myocardial infarction in mice. Am J Physiol Heart Circ Physiol. 2010;298:H1072–8.PubMedCrossRef Nishioka T, Onishi K, Shimojo N, Nagano Y, Matsusaka H, Ikeuchi M, et al. Tenascin-C may aggravate left ventricular remodeling and function after myocardial infarction in mice. Am J Physiol Heart Circ Physiol. 2010;298:H1072–8.PubMedCrossRef
141.
go back to reference Babelova A, Moreth K, Tsalastra-Greul W, Zeng-Brouwers J, Eickelberg O, Young MF, et al. Biglycan, a danger signal that activates the NLRP3 inflammasome via toll-like and P2X receptors. J Biol Chem. 2009;284:24035–48.PubMedPubMedCentralCrossRef Babelova A, Moreth K, Tsalastra-Greul W, Zeng-Brouwers J, Eickelberg O, Young MF, et al. Biglycan, a danger signal that activates the NLRP3 inflammasome via toll-like and P2X receptors. J Biol Chem. 2009;284:24035–48.PubMedPubMedCentralCrossRef
142.
go back to reference Franchi L, Eigenbrod T, Nunez G. Cutting edge: TNF-alpha mediates sensitization to ATP and silica via the NLRP3 inflammasome in the absence of microbial stimulation. J Immunol. 2009;183:792–6.PubMedPubMedCentralCrossRef Franchi L, Eigenbrod T, Nunez G. Cutting edge: TNF-alpha mediates sensitization to ATP and silica via the NLRP3 inflammasome in the absence of microbial stimulation. J Immunol. 2009;183:792–6.PubMedPubMedCentralCrossRef
143.
go back to reference • Sutterwala FS, Haasken S, Cassel SL. Mechanism of NLRP3 inflammasome activation. Ann N Y Acad Sci. 2014;1319:82–95. This comprehensive review highlights our current understanding of the mechanisms of both priming and activation of the NLRP3 inflammasome. • Sutterwala FS, Haasken S, Cassel SL. Mechanism of NLRP3 inflammasome activation. Ann N Y Acad Sci. 2014;1319:82–95. This comprehensive review highlights our current understanding of the mechanisms of both priming and activation of the NLRP3 inflammasome.
144.
go back to reference Zhou R, Yazdi AS, Menu P, Tschopp J. A role for mitochondria in NLRP3 inflammasome activation. Nature. 2011;469:221–5.PubMedCrossRef Zhou R, Yazdi AS, Menu P, Tschopp J. A role for mitochondria in NLRP3 inflammasome activation. Nature. 2011;469:221–5.PubMedCrossRef
145.
go back to reference Lymperopoulos A, Rengo G, Koch WJ. Adrenergic nervous system in heart failure: pathophysiology and therapy. Circ Res. 2013;113:739–53.PubMedCrossRef Lymperopoulos A, Rengo G, Koch WJ. Adrenergic nervous system in heart failure: pathophysiology and therapy. Circ Res. 2013;113:739–53.PubMedCrossRef
146.
go back to reference Pavo N, Wurm R, Goliasch G, Novak JF, Strunk G, Gyongyosi M, et al. Renin-angiotensin system fingerprints of heart failure with reduced ejection fraction. J Am Coll Cardiol. 2016;68:2912–4.PubMedCrossRef Pavo N, Wurm R, Goliasch G, Novak JF, Strunk G, Gyongyosi M, et al. Renin-angiotensin system fingerprints of heart failure with reduced ejection fraction. J Am Coll Cardiol. 2016;68:2912–4.PubMedCrossRef
147.
148.
go back to reference Serbina NV, Pamer EG. Monocyte emigration from bone marrow during bacterial infection requires signals mediated by chemokine receptor CCR2. Nat Immunol. 2006;7:311–7.PubMedCrossRef Serbina NV, Pamer EG. Monocyte emigration from bone marrow during bacterial infection requires signals mediated by chemokine receptor CCR2. Nat Immunol. 2006;7:311–7.PubMedCrossRef
149.
go back to reference Leuschner F, Rauch PJ, Ueno T, Gorbatov R, Marinelli B, Lee WW, et al. Rapid monocyte kinetics in acute myocardial infarction are sustained by extramedullary monocytopoiesis. J Exp Med. 2012;209:123–37.PubMedPubMedCentralCrossRef Leuschner F, Rauch PJ, Ueno T, Gorbatov R, Marinelli B, Lee WW, et al. Rapid monocyte kinetics in acute myocardial infarction are sustained by extramedullary monocytopoiesis. J Exp Med. 2012;209:123–37.PubMedPubMedCentralCrossRef
150.
go back to reference Han Y, Jing J, Tu S, Tian F, Xue H, Chen W, et al. ST elevation acute myocardial infarction accelerates non-culprit coronary lesion atherosclerosis. Int J Cardiovasc Imaging. 2014;30:253–61.PubMedCrossRef Han Y, Jing J, Tu S, Tian F, Xue H, Chen W, et al. ST elevation acute myocardial infarction accelerates non-culprit coronary lesion atherosclerosis. Int J Cardiovasc Imaging. 2014;30:253–61.PubMedCrossRef
151.
go back to reference Nahrendorf M, Swirski FK. Innate immune cells in ischaemic heart disease: does myocardial infarction beget myocardial infarction? Eur Heart J. 2016;37:868–72.PubMedCrossRef Nahrendorf M, Swirski FK. Innate immune cells in ischaemic heart disease: does myocardial infarction beget myocardial infarction? Eur Heart J. 2016;37:868–72.PubMedCrossRef
152.
go back to reference Nilsson KR, Duscha BD, Hranitzky PM, Kraus WE. Chronic heart failure and exercise intolerance: the hemodynamic paradox. Curr Cardiol Rev. 2008;4:92–100.PubMedPubMedCentralCrossRef Nilsson KR, Duscha BD, Hranitzky PM, Kraus WE. Chronic heart failure and exercise intolerance: the hemodynamic paradox. Curr Cardiol Rev. 2008;4:92–100.PubMedPubMedCentralCrossRef
153.
go back to reference Batista ML Jr, Rosa JC, Lopes RD, Lira FS, Martins E Jr, Yamashita AS, et al. Exercise training changes IL-10/TNF-alpha ratio in the skeletal muscle of post-MI rats. Cytokine. 2010;49:102–8.PubMedCrossRef Batista ML Jr, Rosa JC, Lopes RD, Lira FS, Martins E Jr, Yamashita AS, et al. Exercise training changes IL-10/TNF-alpha ratio in the skeletal muscle of post-MI rats. Cytokine. 2010;49:102–8.PubMedCrossRef
154.
go back to reference Gielen S, Adams V, Mobius-Winkler S, Linke A, Erbs S, Yu J, et al. Anti-inflammatory effects of exercise training in the skeletal muscle of patients with chronic heart failure. J Am Coll Cardiol. 2003;42:861–8.PubMedCrossRef Gielen S, Adams V, Mobius-Winkler S, Linke A, Erbs S, Yu J, et al. Anti-inflammatory effects of exercise training in the skeletal muscle of patients with chronic heart failure. J Am Coll Cardiol. 2003;42:861–8.PubMedCrossRef
155.
go back to reference Rossato DD, Dal Lago P, Hentschke VS, Rucatti AL, Signori LU, Silveira MN, et al. Ultrasound modulates skeletal muscle cytokine levels in rats with heart failure. Ultrasound Med Biol. 2015;41:797–805.PubMedCrossRef Rossato DD, Dal Lago P, Hentschke VS, Rucatti AL, Signori LU, Silveira MN, et al. Ultrasound modulates skeletal muscle cytokine levels in rats with heart failure. Ultrasound Med Biol. 2015;41:797–805.PubMedCrossRef
156.
go back to reference Saghizadeh M, Ong JM, Garvey WT, Henry RR, Kern PA. The expression of TNF alpha by human muscle. Relationship to insulin resistance. J Clin Invest. 1996;97:1111–6.PubMedPubMedCentralCrossRef Saghizadeh M, Ong JM, Garvey WT, Henry RR, Kern PA. The expression of TNF alpha by human muscle. Relationship to insulin resistance. J Clin Invest. 1996;97:1111–6.PubMedPubMedCentralCrossRef
157.
go back to reference Van Berendoncks AM, Garnier A, Beckers P, Hoymans VY, Possemiers N, Fortin D, et al. Functional adiponectin resistance at the level of the skeletal muscle in mild to moderate chronic heart failure. Circ Heart Fail. 2010;3:185–94.PubMedCrossRef Van Berendoncks AM, Garnier A, Beckers P, Hoymans VY, Possemiers N, Fortin D, et al. Functional adiponectin resistance at the level of the skeletal muscle in mild to moderate chronic heart failure. Circ Heart Fail. 2010;3:185–94.PubMedCrossRef
158.
go back to reference Seiler M, Bowen TS, Rolim N, Dieterlen MT, Werner S, Hoshi T, et al. Skeletal muscle alterations are exacerbated in heart failure with reduced compared with preserved ejection fraction: mediated by circulating cytokines? Circ Heart Fail. 2016;9 Seiler M, Bowen TS, Rolim N, Dieterlen MT, Werner S, Hoshi T, et al. Skeletal muscle alterations are exacerbated in heart failure with reduced compared with preserved ejection fraction: mediated by circulating cytokines? Circ Heart Fail. 2016;9
159.
go back to reference Tsutsui H, Ide T, Hayashidani S, Suematsu N, Shiomi T, Wen J, et al. Enhanced generation of reactive oxygen species in the limb skeletal muscles from a murine infarct model of heart failure. Circulation. 2001;104:134–6.PubMedCrossRef Tsutsui H, Ide T, Hayashidani S, Suematsu N, Shiomi T, Wen J, et al. Enhanced generation of reactive oxygen species in the limb skeletal muscles from a murine infarct model of heart failure. Circulation. 2001;104:134–6.PubMedCrossRef
160.
go back to reference Clark AL, Poole-Wilson PA, Coats AJ. Exercise limitation in chronic heart failure: central role of the periphery. J Am Coll Cardiol. 1996;28:1092–102.PubMedCrossRef Clark AL, Poole-Wilson PA, Coats AJ. Exercise limitation in chronic heart failure: central role of the periphery. J Am Coll Cardiol. 1996;28:1092–102.PubMedCrossRef
161.
go back to reference Hambrecht R, Gielen S, Linke A, Fiehn E, Yu J, Walther C, et al. Effects of exercise training on left ventricular function and peripheral resistance in patients with chronic heart failure: a randomized trial. JAMA. 2000;283:3095–101.PubMedCrossRef Hambrecht R, Gielen S, Linke A, Fiehn E, Yu J, Walther C, et al. Effects of exercise training on left ventricular function and peripheral resistance in patients with chronic heart failure: a randomized trial. JAMA. 2000;283:3095–101.PubMedCrossRef
162.
go back to reference Wang B, Jenkins JR, Trayhurn P. Expression and secretion of inflammation-related adipokines by human adipocytes differentiated in culture: integrated response to TNF-alpha. Am J Physiol Endocrinol Metab. 2005;288:E731–40.PubMedCrossRef Wang B, Jenkins JR, Trayhurn P. Expression and secretion of inflammation-related adipokines by human adipocytes differentiated in culture: integrated response to TNF-alpha. Am J Physiol Endocrinol Metab. 2005;288:E731–40.PubMedCrossRef
163.
go back to reference Van Linthout S, Foryst-Ludwig A, Spillmann F, Peng J, Feng Y, Meloni M, et al. Impact of HDL on adipose tissue metabolism and adiponectin expression. Atherosclerosis. 2010;210:438–44.PubMedCrossRef Van Linthout S, Foryst-Ludwig A, Spillmann F, Peng J, Feng Y, Meloni M, et al. Impact of HDL on adipose tissue metabolism and adiponectin expression. Atherosclerosis. 2010;210:438–44.PubMedCrossRef
164.
go back to reference Pilz S, Mangge H, Wellnitz B, Seelhorst U, Winkelmann BR, Tiran B, et al. Adiponectin and mortality in patients undergoing coronary angiography. J Clin Endocrinol Metab. 2006;91:4277–86.PubMedCrossRef Pilz S, Mangge H, Wellnitz B, Seelhorst U, Winkelmann BR, Tiran B, et al. Adiponectin and mortality in patients undergoing coronary angiography. J Clin Endocrinol Metab. 2006;91:4277–86.PubMedCrossRef
165.
go back to reference Ozgen M, Koca SS, Dagli N, Balin M, Ustundag B, Isik A. Serum adiponectin and vaspin levels in rheumatoid arthritis. Arch Med Res. 2010;41:457–63.PubMedCrossRef Ozgen M, Koca SS, Dagli N, Balin M, Ustundag B, Isik A. Serum adiponectin and vaspin levels in rheumatoid arthritis. Arch Med Res. 2010;41:457–63.PubMedCrossRef
166.
go back to reference Antonopoulos AS, Margaritis M, Coutinho P, Digby J, Patel R, Psarros C, et al. Reciprocal effects of systemic inflammation and brain natriuretic peptide on adiponectin biosynthesis in adipose tissue of patients with ischemic heart disease. Arterioscler Thromb Vasc Biol. 2014;34:2151–9.PubMedCrossRef Antonopoulos AS, Margaritis M, Coutinho P, Digby J, Patel R, Psarros C, et al. Reciprocal effects of systemic inflammation and brain natriuretic peptide on adiponectin biosynthesis in adipose tissue of patients with ischemic heart disease. Arterioscler Thromb Vasc Biol. 2014;34:2151–9.PubMedCrossRef
167.
go back to reference Koenig W, Khuseyinova N, Baumert J, Meisinger C, Lowel H. Serum concentrations of adiponectin and risk of type 2 diabetes mellitus and coronary heart disease in apparently healthy middle-aged men: results from the 18-year follow-up of a large cohort from southern Germany. J Am Coll Cardiol. 2006;48:1369–77.PubMedCrossRef Koenig W, Khuseyinova N, Baumert J, Meisinger C, Lowel H. Serum concentrations of adiponectin and risk of type 2 diabetes mellitus and coronary heart disease in apparently healthy middle-aged men: results from the 18-year follow-up of a large cohort from southern Germany. J Am Coll Cardiol. 2006;48:1369–77.PubMedCrossRef
168.
go back to reference Tsukamoto O, Fujita M, Kato M, Yamazaki S, Asano Y, Ogai A, et al. Natriuretic peptides enhance the production of adiponectin in human adipocytes and in patients with chronic heart failure. J Am Coll Cardiol. 2009;53:2070–7.PubMedCrossRef Tsukamoto O, Fujita M, Kato M, Yamazaki S, Asano Y, Ogai A, et al. Natriuretic peptides enhance the production of adiponectin in human adipocytes and in patients with chronic heart failure. J Am Coll Cardiol. 2009;53:2070–7.PubMedCrossRef
169.
go back to reference Valero-Munoz M, Li S, Wilson RM, Hulsmans M, Aprahamian T, Fuster JJ, et al. Heart failure with preserved ejection fraction induces beiging in adipose tissue. Circ Heart Fail. 2016;9:e002724.PubMedPubMedCentralCrossRef Valero-Munoz M, Li S, Wilson RM, Hulsmans M, Aprahamian T, Fuster JJ, et al. Heart failure with preserved ejection fraction induces beiging in adipose tissue. Circ Heart Fail. 2016;9:e002724.PubMedPubMedCentralCrossRef
170.
go back to reference Talukdar S, Oh DY, Bandyopadhyay G, Li D, Xu J, McNelis J, et al. Neutrophils mediate insulin resistance in mice fed a high-fat diet through secreted elastase. Nat Med. 2012;18:1407–12.PubMedPubMedCentralCrossRef Talukdar S, Oh DY, Bandyopadhyay G, Li D, Xu J, McNelis J, et al. Neutrophils mediate insulin resistance in mice fed a high-fat diet through secreted elastase. Nat Med. 2012;18:1407–12.PubMedPubMedCentralCrossRef
172.
go back to reference Krack A, Richartz BM, Gastmann A, Greim K, Lotze U, Anker SD, et al. Studies on intragastric PCO2 at rest and during exercise as a marker of intestinal perfusion in patients with chronic heart failure. Eur J Heart Fail. 2004;6:403–7.PubMedCrossRef Krack A, Richartz BM, Gastmann A, Greim K, Lotze U, Anker SD, et al. Studies on intragastric PCO2 at rest and during exercise as a marker of intestinal perfusion in patients with chronic heart failure. Eur J Heart Fail. 2004;6:403–7.PubMedCrossRef
173.
go back to reference Pasini E, Aquilani R, Testa C, Baiardi P, Angioletti S, Boschi F, et al. Pathogenic gut flora in patients with chronic heart failure. JACC Heart Fail. 2016;4:220–7.PubMedCrossRef Pasini E, Aquilani R, Testa C, Baiardi P, Angioletti S, Boschi F, et al. Pathogenic gut flora in patients with chronic heart failure. JACC Heart Fail. 2016;4:220–7.PubMedCrossRef
174.
175.
go back to reference Spengler RN, Allen RM, Remick DG, Strieter RM, Kunkel SL. Stimulation of alpha-adrenergic receptor augments the production of macrophage-derived tumor necrosis factor. J Immunol. 1990;145:1430–4.PubMed Spengler RN, Allen RM, Remick DG, Strieter RM, Kunkel SL. Stimulation of alpha-adrenergic receptor augments the production of macrophage-derived tumor necrosis factor. J Immunol. 1990;145:1430–4.PubMed
176.
go back to reference Chelmicka-Schorr E, Kwasniewski MN, Czlonkowska A. Sympathetic nervous system and macrophage function. Ann N Y Acad Sci. 1992;650:40–5.PubMedCrossRef Chelmicka-Schorr E, Kwasniewski MN, Czlonkowska A. Sympathetic nervous system and macrophage function. Ann N Y Acad Sci. 1992;650:40–5.PubMedCrossRef
177.
178.
go back to reference Vargas AJ, Harris CC. Biomarker development in the precision medicine era: lung cancer as a case study. Nat Rev Cancer. 2016;16:525–37.PubMedCrossRef Vargas AJ, Harris CC. Biomarker development in the precision medicine era: lung cancer as a case study. Nat Rev Cancer. 2016;16:525–37.PubMedCrossRef
Metadata
Title
Inflammation – Cause or Consequence of Heart Failure or Both?
Authors
Sophie Van Linthout
Carsten Tschöpe
Publication date
01-08-2017
Publisher
Springer US
Published in
Current Heart Failure Reports / Issue 4/2017
Print ISSN: 1546-9530
Electronic ISSN: 1546-9549
DOI
https://doi.org/10.1007/s11897-017-0337-9

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