Skip to main content
Top
Published in: Current Osteoporosis Reports 2/2014

01-06-2014 | Muscle and Bone (L Bonewald and M Harrick, Section Editors)

Endocrine Crosstalk Between Muscle and Bone

Authors: Marco Brotto, Mark L. Johnson

Published in: Current Osteoporosis Reports | Issue 2/2014

Login to get access

Abstract

The musculoskeletal system is a complex organ comprised of the skeletal bones, skeletal muscles, tendons, ligaments, cartilage, joints, and other connective tissue that physically and mechanically interact to provide animals and humans with the essential ability of locomotion. This mechanical interaction is undoubtedly essential for much of the diverse shape and forms observed in vertebrates and even in invertebrates with rudimentary musculoskeletal systems such as fish. It makes sense from a historical point of view that the mechanical theories of musculoskeletal development have had tremendous influence of our understanding of biology, because these relationships are clear and palpable. Less visible to the naked eye or even to the microscope is the biochemical interaction among the individual players of the musculoskeletal system. It was only in recent years that we have begun to appreciate that beyond this mechanical coupling of muscle and bones, these 2 tissues function at a higher level through crosstalk signaling mechanisms that are important for the function of the concomitant tissue. Our brief review attempts to present some of the key concepts of these new concepts and is outline to present muscles and bones as secretory/endocrine organs, the evidence for mutual genetic and tissue interactions, pathophysiological examples of crosstalk, and the exciting new directions for this promising field of research aimed at understanding the biochemical/molecular coupling of these 2 intimately associated tissues.
Literature
2.
go back to reference Rauch F, Schoenau E. The developing bone: slave or master of its cells and molecules? Pediatr Res. 2001;50:309–14.PubMedCrossRef Rauch F, Schoenau E. The developing bone: slave or master of its cells and molecules? Pediatr Res. 2001;50:309–14.PubMedCrossRef
3.
go back to reference Land C, Schoenau E. Fetal and postnatal bone development: reviewing the role of mechanical stimuli and nutrition. Best Pract Res Clin Endocrinol Metab. 2008;22:107–18.PubMedCrossRef Land C, Schoenau E. Fetal and postnatal bone development: reviewing the role of mechanical stimuli and nutrition. Best Pract Res Clin Endocrinol Metab. 2008;22:107–18.PubMedCrossRef
5.
go back to reference Recker R, Lappe J, Davies K, Heaney R. Characterization of peri-menopausal bone loss: a prospective study. J Bone Miner Res. 2000;15:1965–73.PubMedCrossRef Recker R, Lappe J, Davies K, Heaney R. Characterization of peri-menopausal bone loss: a prospective study. J Bone Miner Res. 2000;15:1965–73.PubMedCrossRef
6.
go back to reference Hu MC, Shiizaki K, Kuro-o M, Moe OW. Fibroblast growth factor 23 and klotho: physiology and pathophysiology of an endocrine network of mineral metabolism. Annu Rev Physiol. 2013;75:503–33.PubMedCentralPubMedCrossRef Hu MC, Shiizaki K, Kuro-o M, Moe OW. Fibroblast growth factor 23 and klotho: physiology and pathophysiology of an endocrine network of mineral metabolism. Annu Rev Physiol. 2013;75:503–33.PubMedCentralPubMedCrossRef
7.
go back to reference Kurek JB et al. The role of leukemia inhibitory factor in skeletal muscle regeneration. Muscle Nerve. 1997;20:815–22.PubMedCrossRef Kurek JB et al. The role of leukemia inhibitory factor in skeletal muscle regeneration. Muscle Nerve. 1997;20:815–22.PubMedCrossRef
8.
go back to reference Allen DL et al. Myostatin, activin receptor IIb, and follistatin-like-3 gene expression are altered in adipose tissue and skeletal muscle of obese mice. Am J Physiol Endocrinol Metab. 2008;294:E918–27.PubMedCrossRef Allen DL et al. Myostatin, activin receptor IIb, and follistatin-like-3 gene expression are altered in adipose tissue and skeletal muscle of obese mice. Am J Physiol Endocrinol Metab. 2008;294:E918–27.PubMedCrossRef
9.••
go back to reference Pedersen BK. Muscle as a secretory organ. Compr Physiol. 2013;3:1337–62. The discovery of Myostatin as the first muscle secreted factor was a landmark in the fields of muscle and musculoskeletal research. This discovery opened the door for the thinking that secreted factors from muscles could have organismal effects. Also, myostatin became known as the most important negative regulator of muscle mass. PubMed Pedersen BK. Muscle as a secretory organ. Compr Physiol. 2013;3:1337–62. The discovery of Myostatin as the first muscle secreted factor was a landmark in the fields of muscle and musculoskeletal research. This discovery opened the door for the thinking that secreted factors from muscles could have organismal effects. Also, myostatin became known as the most important negative regulator of muscle mass. PubMed
10.
go back to reference Allen DL, Hittel DS, McPherron AC. Expression and function of myostatin in obesity, diabetes, and exercise adaptation. Med Sci Sports Exerc. 2011;43:1828–35.PubMedCentralPubMedCrossRef Allen DL, Hittel DS, McPherron AC. Expression and function of myostatin in obesity, diabetes, and exercise adaptation. Med Sci Sports Exerc. 2011;43:1828–35.PubMedCentralPubMedCrossRef
11.
go back to reference Pedersen BK et al. Searching for the exercise factor: is IL-6 a candidate. J Muscle Res Cell Motil. 2003;24:113–9.PubMedCrossRef Pedersen BK et al. Searching for the exercise factor: is IL-6 a candidate. J Muscle Res Cell Motil. 2003;24:113–9.PubMedCrossRef
12.
go back to reference Reihmane D, Jurka A, Tretjakos P, Dela F. Increase in IL-6, TNF-a, and MMP-9, but not sICAM-1, concentrations depends on exercise duration. Eur J Appl Physiol. 2013;113:851–88.PubMedCrossRef Reihmane D, Jurka A, Tretjakos P, Dela F. Increase in IL-6, TNF-a, and MMP-9, but not sICAM-1, concentrations depends on exercise duration. Eur J Appl Physiol. 2013;113:851–88.PubMedCrossRef
13.
go back to reference Libardi CA, De Souza GV, Cavaglieri CR, Madruga VA, Chacon-Mikahil MP. Effect of resistance, endurance, and concurrent training on TNF-a, IL-6, and CRP. Med Sci Sports Exerc. 2012;44:50–5.PubMedCrossRef Libardi CA, De Souza GV, Cavaglieri CR, Madruga VA, Chacon-Mikahil MP. Effect of resistance, endurance, and concurrent training on TNF-a, IL-6, and CRP. Med Sci Sports Exerc. 2012;44:50–5.PubMedCrossRef
14.
go back to reference Matthews VB et al. Brain-derived neurotrophic factor is produced by skeletal muscle cells in response to contraction and enhances fat oxidation via activation of AMP-activated protein kinase. Diabetologia. 2009;52:1409–18.PubMedCrossRef Matthews VB et al. Brain-derived neurotrophic factor is produced by skeletal muscle cells in response to contraction and enhances fat oxidation via activation of AMP-activated protein kinase. Diabetologia. 2009;52:1409–18.PubMedCrossRef
15.
go back to reference Pedersen BK, Akerstrom TC, Nielsen AR, Fischer CP. Role of myokines in exercise and metabolism. J Appl Physiol. 2007;103(3):1093–8. Pedersen BK, Akerstrom TC, Nielsen AR, Fischer CP. Role of myokines in exercise and metabolism. J Appl Physiol. 2007;103(3):1093–8.
16.
go back to reference Pedersen L, Olsen CH, Pedersen BK, Hojman P. Muscle-derived expression of the chemokine CXCL1 attenuates diet-induced obesity and improves fatty acid oxidation in the muscle. Am J Physiol Endocrinol Metab. 2012;302:E831–40.PubMedCrossRef Pedersen L, Olsen CH, Pedersen BK, Hojman P. Muscle-derived expression of the chemokine CXCL1 attenuates diet-induced obesity and improves fatty acid oxidation in the muscle. Am J Physiol Endocrinol Metab. 2012;302:E831–40.PubMedCrossRef
18.•
go back to reference Quinn LS, Anderson BG, Strait-Bodey L, Stroud AM, Argiles JM. Oversecretion of interleukin-15 from skeletal muscle reduces adiposity. Am J Physiol Endocrinol Metab. 2009;296:E191–202. The demonstration that the overexpression of a muscle specific myokine could alter adiposity and also increase BMD is a remarkable indication that muscle can signal to bone in a biochemical manner. PubMedCentralPubMedCrossRef Quinn LS, Anderson BG, Strait-Bodey L, Stroud AM, Argiles JM. Oversecretion of interleukin-15 from skeletal muscle reduces adiposity. Am J Physiol Endocrinol Metab. 2009;296:E191–202. The demonstration that the overexpression of a muscle specific myokine could alter adiposity and also increase BMD is a remarkable indication that muscle can signal to bone in a biochemical manner. PubMedCentralPubMedCrossRef
19.
go back to reference Hee Park K et al. Circulating irisin in relation to insulin resistance and the metabolic syndrome. J Clin Endocrinol Metab. 2013;98:4899–907.CrossRef Hee Park K et al. Circulating irisin in relation to insulin resistance and the metabolic syndrome. J Clin Endocrinol Metab. 2013;98:4899–907.CrossRef
20.
go back to reference Bortoluzzi S, Scannapieco P, Cestaro A, Danieli GA, Schiaffino S. Computational reconstruction of the human skeletal muscle secretome. Proteins. 2006;62:776–92.PubMedCrossRef Bortoluzzi S, Scannapieco P, Cestaro A, Danieli GA, Schiaffino S. Computational reconstruction of the human skeletal muscle secretome. Proteins. 2006;62:776–92.PubMedCrossRef
21.
go back to reference Pedersen BK, Febbraio MA. Muscles, exercise and obesity: skeletal muscle as a secretory organ. Nat Rev Endocrinol. 2012;8:457–65.PubMedCrossRef Pedersen BK, Febbraio MA. Muscles, exercise and obesity: skeletal muscle as a secretory organ. Nat Rev Endocrinol. 2012;8:457–65.PubMedCrossRef
23.
go back to reference Lee NK, Karsenty G. Reciprocal regulation of bone and energy metabolism. Trends Endocrinol Metabol. 2008;19:161–6.CrossRef Lee NK, Karsenty G. Reciprocal regulation of bone and energy metabolism. Trends Endocrinol Metabol. 2008;19:161–6.CrossRef
24.
go back to reference DiGirolamo DJ, Clemens TL, Kousteni S. The skeleton as an endocrine organ. Nat Rev Rheumatol. 2012;8:674–83.PubMedCrossRef DiGirolamo DJ, Clemens TL, Kousteni S. The skeleton as an endocrine organ. Nat Rev Rheumatol. 2012;8:674–83.PubMedCrossRef
25.
go back to reference Guntar AR, Rosen CJ. Bone as an Endocrine Organ. Endocr Pract. 2012;18:758–62.CrossRef Guntar AR, Rosen CJ. Bone as an Endocrine Organ. Endocr Pract. 2012;18:758–62.CrossRef
27.
go back to reference Schwetz V, Pieber T, Obermayer-Pietsch B. Mechanisms in endocrinology: the endocrine role of the skeleton: background and clinical evidence. Eur J Endocrinol. 2012;166:959–67.PubMedCrossRef Schwetz V, Pieber T, Obermayer-Pietsch B. Mechanisms in endocrinology: the endocrine role of the skeleton: background and clinical evidence. Eur J Endocrinol. 2012;166:959–67.PubMedCrossRef
28.
go back to reference Karsenty G, Ferron M. The contribution of bone to whole-organism physiology. Nature. 2012;481:314–20.PubMedCrossRef Karsenty G, Ferron M. The contribution of bone to whole-organism physiology. Nature. 2012;481:314–20.PubMedCrossRef
29.
go back to reference Quarles LD. Skeletal secretion of FGF-23 regulates phosphate and vitamin D metabolism. Nat Rev Endocrinol. 2012;8:276–86.PubMedCrossRef Quarles LD. Skeletal secretion of FGF-23 regulates phosphate and vitamin D metabolism. Nat Rev Endocrinol. 2012;8:276–86.PubMedCrossRef
30.
go back to reference Neve A, Corrado A, Cantatore FP. Osteocytes: central conductors of bone biology in normal and pathological conditions. Acta Physiol. 2012;204:317–30.CrossRef Neve A, Corrado A, Cantatore FP. Osteocytes: central conductors of bone biology in normal and pathological conditions. Acta Physiol. 2012;204:317–30.CrossRef
31.
go back to reference Econs MJ et al. A PHEX Gene mutation is responsible for adult-onset Vitamin D-resistant hypophosphatemic osteomalacia: evidence that the disorder is not a distinct entity from X-Linked Hypophosphatemic Rickets. J Clin Endocrinol Metab. 1998;83:3459–62.PubMed Econs MJ et al. A PHEX Gene mutation is responsible for adult-onset Vitamin D-resistant hypophosphatemic osteomalacia: evidence that the disorder is not a distinct entity from X-Linked Hypophosphatemic Rickets. J Clin Endocrinol Metab. 1998;83:3459–62.PubMed
32.
go back to reference Dallas SL, Prideaux M, Bonewald LF. The osteocyte: an endocrine cell. … and more. Endocr Rev. 2013;34:658–90.PubMedCrossRef Dallas SL, Prideaux M, Bonewald LF. The osteocyte: an endocrine cell. … and more. Endocr Rev. 2013;34:658–90.PubMedCrossRef
33.
go back to reference The ADHR Consortium. Autosomal dominant hypophosphataemic rickets is associated with mutations in FGF23. Nat Genet. 2000;26:345–8.CrossRef The ADHR Consortium. Autosomal dominant hypophosphataemic rickets is associated with mutations in FGF23. Nat Genet. 2000;26:345–8.CrossRef
34.
go back to reference Quarles LD. FGF23, PHEX, and MEPE regulation of phosphate homeostasis and skeletal mineralization. Am J Physiol Endocrinol Metab. 2003;285:E1–9.PubMed Quarles LD. FGF23, PHEX, and MEPE regulation of phosphate homeostasis and skeletal mineralization. Am J Physiol Endocrinol Metab. 2003;285:E1–9.PubMed
35.
go back to reference Liu S et al. Pathogenic role of Fgf23 in Hyp mice. Am J Physiol Endocrinol Metab. 2006;291:E38–49.PubMedCrossRef Liu S et al. Pathogenic role of Fgf23 in Hyp mice. Am J Physiol Endocrinol Metab. 2006;291:E38–49.PubMedCrossRef
36.
go back to reference Francis F et al. A gene (PEX) with homologies to endopeptidases is mutated in patients with X-linked hypophosphatemic rickets. Nat Genet. 1995;11:130–6.CrossRef Francis F et al. A gene (PEX) with homologies to endopeptidases is mutated in patients with X-linked hypophosphatemic rickets. Nat Genet. 1995;11:130–6.CrossRef
37.
go back to reference Rowe PSN et al. Distribution of Mutations in the PEX Gene in Families with X-linked Hypophosphataemic Rickets (HYP). Hum Molec Genet. 1997;6:539–49.PubMedCrossRef Rowe PSN et al. Distribution of Mutations in the PEX Gene in Families with X-linked Hypophosphataemic Rickets (HYP). Hum Molec Genet. 1997;6:539–49.PubMedCrossRef
38.
go back to reference Dixon PH et al. Mutational analysis of PHEX gene in X-Linked Hypophosphatemia. J Clin Endocrinol Metab. 1998;83:3615–23.PubMed Dixon PH et al. Mutational analysis of PHEX gene in X-Linked Hypophosphatemia. J Clin Endocrinol Metab. 1998;83:3615–23.PubMed
40.
go back to reference Touchberry CD et al. FGF23 is a novel regulator of intracellular calcium and cardiac contractility in addition to cardiac hypertrophy. Am J Physiol Endocrinol Metab. 2013;304:E863–73.PubMedCentralPubMedCrossRef Touchberry CD et al. FGF23 is a novel regulator of intracellular calcium and cardiac contractility in addition to cardiac hypertrophy. Am J Physiol Endocrinol Metab. 2013;304:E863–73.PubMedCentralPubMedCrossRef
42.
go back to reference Frost HM. Bone's Mechanostat: a 2003 update. Anat Rec. 2003;275A:1081–101.CrossRef Frost HM. Bone's Mechanostat: a 2003 update. Anat Rec. 2003;275A:1081–101.CrossRef
43.
go back to reference Arden NK, Spector TD. Genetic influences on muscle strength, lean body mass, and bone mineral density: a twin study. J Bone Miner Res. 1997;12:2076–81.PubMedCrossRef Arden NK, Spector TD. Genetic influences on muscle strength, lean body mass, and bone mineral density: a twin study. J Bone Miner Res. 1997;12:2076–81.PubMedCrossRef
44.
go back to reference Silventoinen K, Magnusson PKE, Tynelius P, Kaprio J, Rasmussen F. Heritability of body size and muscle strength in young adulthood: a study of one million Swedish men. Genet Epidemiol. 2008;32:341–9.PubMedCrossRef Silventoinen K, Magnusson PKE, Tynelius P, Kaprio J, Rasmussen F. Heritability of body size and muscle strength in young adulthood: a study of one million Swedish men. Genet Epidemiol. 2008;32:341–9.PubMedCrossRef
45.
go back to reference Prior SJ et al. Genetic and environmental influences on skeletal muscle phenotypes as a function of age and sex in large, multigenerational families of African heritage. J Appl Physiol. 2007;103:1121–7. Prior SJ et al. Genetic and environmental influences on skeletal muscle phenotypes as a function of age and sex in large, multigenerational families of African heritage. J Appl Physiol. 2007;103:1121–7.
46.
go back to reference Costa A et al. Genetic inheritance effects on endurance and muscle strength. Sports Med. 2012;42:449–58.PubMedCrossRef Costa A et al. Genetic inheritance effects on endurance and muscle strength. Sports Med. 2012;42:449–58.PubMedCrossRef
47.
go back to reference Rivadeneira F et al. Twenty bone-mineral-density loci identified by large-scale meta-analysis of genome-wide association studies. Nat Genet. 2009;41:1199–206.PubMedCentralPubMedCrossRef Rivadeneira F et al. Twenty bone-mineral-density loci identified by large-scale meta-analysis of genome-wide association studies. Nat Genet. 2009;41:1199–206.PubMedCentralPubMedCrossRef
49.
go back to reference Duncan EL et al. Genome-wide association study using extreme truncate selection identifies novel genes affecting bone mineral density and fracture risk. PLoS Genet. 2011;7:e1001372.PubMedCentralPubMedCrossRef Duncan EL et al. Genome-wide association study using extreme truncate selection identifies novel genes affecting bone mineral density and fracture risk. PLoS Genet. 2011;7:e1001372.PubMedCentralPubMedCrossRef
50.
go back to reference Estrada K et al. Genome-wide meta-analysis identifies 56 bone mineral density loci and reveals 14 loci associated with risk of fracture. Nat Genet. 2012;44:491–501.PubMedCentralPubMedCrossRef Estrada K et al. Genome-wide meta-analysis identifies 56 bone mineral density loci and reveals 14 loci associated with risk of fracture. Nat Genet. 2012;44:491–501.PubMedCentralPubMedCrossRef
51.
go back to reference Lee Y, Choi S, Ji J, Song G. Pathway analysis of genome-wide association study for bone mineral density. Mol Biol Rep. 2012;39:8099–106.PubMedCrossRef Lee Y, Choi S, Ji J, Song G. Pathway analysis of genome-wide association study for bone mineral density. Mol Biol Rep. 2012;39:8099–106.PubMedCrossRef
52.
go back to reference Ran S et al. Bivariate genome-wide association analyses identified genes with pleiotropic effects for femoral neck bone geometry and age at menarche. PLoS One. 2013;8:e60362.PubMedCentralPubMedCrossRef Ran S et al. Bivariate genome-wide association analyses identified genes with pleiotropic effects for femoral neck bone geometry and age at menarche. PLoS One. 2013;8:e60362.PubMedCentralPubMedCrossRef
54.
go back to reference Zhang L, et al. Multistage genome-wide association meta-analyses identified two new loci for bone mineral density. Hum Mol Genet. 2014;23(7):1923–33. doi:10.1093/hmg/ddt575. Zhang L, et al. Multistage genome-wide association meta-analyses identified two new loci for bone mineral density. Hum Mol Genet. 2014;23(7):1923–33. doi:10.​1093/​hmg/​ddt575.
56.
go back to reference Pérusse L et al. The Human gene map for performance and health-related fitness phenotypes: the 2002 Update. Med Sci Sports Exerc. 2003;35:1248–64.PubMedCrossRef Pérusse L et al. The Human gene map for performance and health-related fitness phenotypes: the 2002 Update. Med Sci Sports Exerc. 2003;35:1248–64.PubMedCrossRef
57.
go back to reference Liu X-G et al. Genome-wide association and replication studies identified TRHR as an important gene for lean body mass. Am J Hum Genet. 2009;84:418–23.PubMedCentralPubMedCrossRef Liu X-G et al. Genome-wide association and replication studies identified TRHR as an important gene for lean body mass. Am J Hum Genet. 2009;84:418–23.PubMedCentralPubMedCrossRef
58.
go back to reference Thomis MA et al. Genome-wide linkage scan for resistance to muscle fatigue. Scand J Med Sci Sports. 2011;21:580–8.PubMedCrossRef Thomis MA et al. Genome-wide linkage scan for resistance to muscle fatigue. Scand J Med Sci Sports. 2011;21:580–8.PubMedCrossRef
59.
go back to reference Windelinckx A et al. Comprehensive fine mapping of chr12q12-14 and follow-up replication identify activin receptor 1B (ACVR1B) as a muscle strength gene. Eur J Hum Genet. 2011;19:208–15.PubMedCentralPubMedCrossRef Windelinckx A et al. Comprehensive fine mapping of chr12q12-14 and follow-up replication identify activin receptor 1B (ACVR1B) as a muscle strength gene. Eur J Hum Genet. 2011;19:208–15.PubMedCentralPubMedCrossRef
60.
go back to reference Hai R et al. Genome-wide association study of copy number variation identified gremlin1 as a candidate gene for lean body mass. J Hum Genet. 2012;57:33–7.PubMedCrossRef Hai R et al. Genome-wide association study of copy number variation identified gremlin1 as a candidate gene for lean body mass. J Hum Genet. 2012;57:33–7.PubMedCrossRef
61.
go back to reference Kuo T et al. Genome-wide analysis of glucocorticoid receptor-binding sites in myotubes identifies gene networks modulating insulin signaling. Proc Natl Acad Sci. 2012;109:11160–5.PubMedCentralPubMedCrossRef Kuo T et al. Genome-wide analysis of glucocorticoid receptor-binding sites in myotubes identifies gene networks modulating insulin signaling. Proc Natl Acad Sci. 2012;109:11160–5.PubMedCentralPubMedCrossRef
62.
go back to reference Guo Y-F et al. Suggestion of GLYAT gene underlying variation of bone size and body lean mass as revealed by a bivariate genome-wide association study. Hum Genet. 2013;132:189–99.PubMedCentralPubMedCrossRef Guo Y-F et al. Suggestion of GLYAT gene underlying variation of bone size and body lean mass as revealed by a bivariate genome-wide association study. Hum Genet. 2013;132:189–99.PubMedCentralPubMedCrossRef
63.
go back to reference Cheng Y et al. Body composition and gene expression QTL mapping in mice reveals imprinting and interaction effects. BMC Genet. 2013;14:103.PubMedCrossRef Cheng Y et al. Body composition and gene expression QTL mapping in mice reveals imprinting and interaction effects. BMC Genet. 2013;14:103.PubMedCrossRef
64.
go back to reference Keildson S, et al. Skeletal muscle expression of phosphofructokinase is influenced by genetic variation and associated with insulin sensitivity. Diabetes. 2014;63(3):1154-65. doi:10.2337/db13-1301. Keildson S, et al. Skeletal muscle expression of phosphofructokinase is influenced by genetic variation and associated with insulin sensitivity. Diabetes. 2014;63(3):1154-65. doi:10.​2337/​db13-1301.
65.
go back to reference Karasik D et al. Bivariate genome-wide linkage analysis of femoral bone traits and leg lean mass: The Framingham Study. J Bone Miner Res. 2009;24:710–8.PubMedCentralPubMedCrossRef Karasik D et al. Bivariate genome-wide linkage analysis of femoral bone traits and leg lean mass: The Framingham Study. J Bone Miner Res. 2009;24:710–8.PubMedCentralPubMedCrossRef
66.
go back to reference Karasik D, Kiel DP. Evidence for pleiotropic factors in genetics of the musculoskeletal system. Bone. 2010;46:1226–37.PubMedCrossRef Karasik D, Kiel DP. Evidence for pleiotropic factors in genetics of the musculoskeletal system. Bone. 2010;46:1226–37.PubMedCrossRef
67.
go back to reference Gupta M et al. Identification of homogeneous genetic architecture of multiple genetically correlated traits by block clustering of genome-wide associations. J Bone Miner Res. 2011;26:1261–71.PubMedCentralPubMedCrossRef Gupta M et al. Identification of homogeneous genetic architecture of multiple genetically correlated traits by block clustering of genome-wide associations. J Bone Miner Res. 2011;26:1261–71.PubMedCentralPubMedCrossRef
69.
go back to reference Karasik D, Cohen-Zinder M. Osteoporosis genetics: year 2011 in review. Bone Key Rep. 2012;1(114):1–5. Karasik D, Cohen-Zinder M. Osteoporosis genetics: year 2011 in review. Bone Key Rep. 2012;1(114):1–5.
70.
go back to reference Edmondson DG, Lyons GE, Martin JF, Olson EN. Mef2 gene expression marks the cardiac and skeletal muscle lineages during mouse embryogenesis. Development. 1994;120:1251–63.PubMed Edmondson DG, Lyons GE, Martin JF, Olson EN. Mef2 gene expression marks the cardiac and skeletal muscle lineages during mouse embryogenesis. Development. 1994;120:1251–63.PubMed
71.
go back to reference Kramer I, Baertschi S, Halleux C, Keller H, Kneissel M. Mef2c deletion in osteocytes results in increased bone mass. J Bone Miner Res. 2012;27:360–73.PubMedCrossRef Kramer I, Baertschi S, Halleux C, Keller H, Kneissel M. Mef2c deletion in osteocytes results in increased bone mass. J Bone Miner Res. 2012;27:360–73.PubMedCrossRef
72.
go back to reference Grobet L et al. A deletion in the bovine myostatin gene causes the double-muscled phenotype in cattle. Nat Genet. 1997;17:71–4.PubMedCrossRef Grobet L et al. A deletion in the bovine myostatin gene causes the double-muscled phenotype in cattle. Nat Genet. 1997;17:71–4.PubMedCrossRef
73.
go back to reference Kambadur R, Sharma M, Smith TPL, Bass JJ. Mutations in myostatin (GDF8) in Double-Muscled Belgian Blue and Piedmontese Cattle. Genome Res. 1997;7:910–5.PubMed Kambadur R, Sharma M, Smith TPL, Bass JJ. Mutations in myostatin (GDF8) in Double-Muscled Belgian Blue and Piedmontese Cattle. Genome Res. 1997;7:910–5.PubMed
75.
go back to reference Clop A et al. A mutation creating a potential illegitimate microRNA target site in the myostatin gene affects muscularity in sheep. Nat Genet. 2006;38:813–8.PubMedCrossRef Clop A et al. A mutation creating a potential illegitimate microRNA target site in the myostatin gene affects muscularity in sheep. Nat Genet. 2006;38:813–8.PubMedCrossRef
76.
77.
go back to reference Zhang GX, Zhao XH, Wang JY, Ding FX, Zhang L. Effect of an exon 1 mutation in the myostatin gene on the growth traits of the Bian chicken. Anim Genet. 2012;43:458–9.PubMedCrossRef Zhang GX, Zhao XH, Wang JY, Ding FX, Zhang L. Effect of an exon 1 mutation in the myostatin gene on the growth traits of the Bian chicken. Anim Genet. 2012;43:458–9.PubMedCrossRef
78.
go back to reference Williams M. Myostatin mutation associated with gross muscle hypertrophy in a child. N Engl J Med. 2004;351:1030–1.PubMedCrossRef Williams M. Myostatin mutation associated with gross muscle hypertrophy in a child. N Engl J Med. 2004;351:1030–1.PubMedCrossRef
79.
go back to reference Pedersen BK, Febbraio MA. Muscles, exercise and obesity: skeletal muscle as a secretory organ. Nat Rev Endocrinol. 2012;8:457–65.PubMedCrossRef Pedersen BK, Febbraio MA. Muscles, exercise and obesity: skeletal muscle as a secretory organ. Nat Rev Endocrinol. 2012;8:457–65.PubMedCrossRef
80.
go back to reference Elkasrawy M, Hamrick M. Myostatin (GDF-8) as a key factor linking muscle mass and bone structure. J Musculoskelet Neuronal Interact. 2010;10:56–63.PubMedCentralPubMed Elkasrawy M, Hamrick M. Myostatin (GDF-8) as a key factor linking muscle mass and bone structure. J Musculoskelet Neuronal Interact. 2010;10:56–63.PubMedCentralPubMed
81.
82.
go back to reference Perrini S et al. The GH/IGF1 axis and signaling pathways in the muscle and bone: mechanisms underlying age-related skeletal muscle wasting and osteoporosis. J Endocrinol. 2010;205:201–10.PubMedCrossRef Perrini S et al. The GH/IGF1 axis and signaling pathways in the muscle and bone: mechanisms underlying age-related skeletal muscle wasting and osteoporosis. J Endocrinol. 2010;205:201–10.PubMedCrossRef
83.
go back to reference Zacks SI, Sheff MF. Periosteal and metaplastic bone formation in mouse minced muscle regeneration. Lab Invest. 1982;46:405–12.PubMed Zacks SI, Sheff MF. Periosteal and metaplastic bone formation in mouse minced muscle regeneration. Lab Invest. 1982;46:405–12.PubMed
84.
go back to reference Landry PS, Marino AA, Sadasivan KK, Albright JA. Effect of soft-tissue trauma on the early periosteal response of bone to injury. J Trauma. 2000;48:479–83.PubMedCrossRef Landry PS, Marino AA, Sadasivan KK, Albright JA. Effect of soft-tissue trauma on the early periosteal response of bone to injury. J Trauma. 2000;48:479–83.PubMedCrossRef
85.
go back to reference Utvag SE, Iversen KB, Grundnes O, Reikeras O. Poor muscle coverage delays fracture healing in rats. Acta Orthop Scand. 2002;73:471–4.PubMedCrossRef Utvag SE, Iversen KB, Grundnes O, Reikeras O. Poor muscle coverage delays fracture healing in rats. Acta Orthop Scand. 2002;73:471–4.PubMedCrossRef
86.
go back to reference Stein H et al. The muscle bed–a crucial factor for fracture healing: a physiological concept. Orthopedics. 2002;25:1379–83.PubMed Stein H et al. The muscle bed–a crucial factor for fracture healing: a physiological concept. Orthopedics. 2002;25:1379–83.PubMed
87.
go back to reference Harry LE et al. Comparison of the healing of open tibial fractures covered with either muscle or fasciocutaneous tissue in a murine model. J Orthop Res. 2008;26:1238–44.PubMedCrossRef Harry LE et al. Comparison of the healing of open tibial fractures covered with either muscle or fasciocutaneous tissue in a murine model. J Orthop Res. 2008;26:1238–44.PubMedCrossRef
88.
go back to reference Gopal S, Majumder AG, Knight SL, De Boer P, Smith RM. Fix and Flap: the radical orthopedic and plastic treatment of severe open fractures of the tibia. J Bone Joint Surg (Br). 2000;82:959–66.CrossRef Gopal S, Majumder AG, Knight SL, De Boer P, Smith RM. Fix and Flap: the radical orthopedic and plastic treatment of severe open fractures of the tibia. J Bone Joint Surg (Br). 2000;82:959–66.CrossRef
89.•
go back to reference Elkasrawy M et al. Immunolocalization of myostatin (GDF-8) following musculoskeletal injury and the effects of exogenous myostatin on muscle and bone healing. J Histochem Cytochem. 2012;60:22–30. This paper demonstrated that by inhibiting myostatin action early in the process of musculoskeletal injury, healing of both muscle and bone could be improved and accelerated. PubMedCentralPubMedCrossRef Elkasrawy M et al. Immunolocalization of myostatin (GDF-8) following musculoskeletal injury and the effects of exogenous myostatin on muscle and bone healing. J Histochem Cytochem. 2012;60:22–30. This paper demonstrated that by inhibiting myostatin action early in the process of musculoskeletal injury, healing of both muscle and bone could be improved and accelerated. PubMedCentralPubMedCrossRef
90.
go back to reference Schindeler A, Liu R, Little DG. The contribution of different cell lineages to bone repair: exploring a role for muscle stem cells. Differentiation. 2009;77:12–8.PubMedCrossRef Schindeler A, Liu R, Little DG. The contribution of different cell lineages to bone repair: exploring a role for muscle stem cells. Differentiation. 2009;77:12–8.PubMedCrossRef
91.
go back to reference Liu R, Schindeler A, Little DG. The potential role of muscle in bone repair. J Musculoskel Neuronal Interact. 2010;10:71–6. Liu R, Schindeler A, Little DG. The potential role of muscle in bone repair. J Musculoskel Neuronal Interact. 2010;10:71–6.
92.
go back to reference Griffin XL, Costa ML, Parsons N, Smith N. Electromagnetic field stimulation for treating delayed union or non-union of long bone fractures in adults. Cochrane Database Syst Rev, 2011;CD008471. Griffin XL, Costa ML, Parsons N, Smith N. Electromagnetic field stimulation for treating delayed union or non-union of long bone fractures in adults. Cochrane Database Syst Rev, 2011;CD008471.
93.
go back to reference Leon-Salas WD et al. A dual mode pulsed electro-magnetic cell stimulator produces acceleration of myogenic differentiation. Recent Pat Biotechnol. 2013;7:71–81.PubMedCentralPubMedCrossRef Leon-Salas WD et al. A dual mode pulsed electro-magnetic cell stimulator produces acceleration of myogenic differentiation. Recent Pat Biotechnol. 2013;7:71–81.PubMedCentralPubMedCrossRef
94.
go back to reference Fakhouri TH, Ogden CL, Carroll MD, Kit BK, Flegal KM. Prevalence of obesity among older adults in the United States, 2007-2010. NCHS Data Brief. 2012;(106):1–8. Fakhouri TH, Ogden CL, Carroll MD, Kit BK, Flegal KM. Prevalence of obesity among older adults in the United States, 2007-2010. NCHS Data Brief. 2012;(106):1–8.
95.
go back to reference Conboy IM et al. Rejuvenation of aged progenitor cells by exposure to a young systemic environment. Nature. 2005;433:760–4.PubMedCrossRef Conboy IM et al. Rejuvenation of aged progenitor cells by exposure to a young systemic environment. Nature. 2005;433:760–4.PubMedCrossRef
96.
go back to reference Jahn K et al. Skeletal muscle secreted factors prevent glucocorticoid-induced osteocyte apoptosis through activation of beta-catenin. Eur Cell Mater. 2012;24:197–209. discussion 209–110.PubMedCentralPubMed Jahn K et al. Skeletal muscle secreted factors prevent glucocorticoid-induced osteocyte apoptosis through activation of beta-catenin. Eur Cell Mater. 2012;24:197–209. discussion 209–110.PubMedCentralPubMed
Metadata
Title
Endocrine Crosstalk Between Muscle and Bone
Authors
Marco Brotto
Mark L. Johnson
Publication date
01-06-2014
Publisher
Springer US
Published in
Current Osteoporosis Reports / Issue 2/2014
Print ISSN: 1544-1873
Electronic ISSN: 1544-2241
DOI
https://doi.org/10.1007/s11914-014-0209-0

Other articles of this Issue 2/2014

Current Osteoporosis Reports 2/2014 Go to the issue

Biomechanics (M Silva and P Zysset, Section Editors)

Atypical Femoral Fractures, Bisphosphonates, and Mechanical Stress

Nutrition, Exercise, and Lifestyle in Osteoporosis (C Weaver and S Ferrari, Section Editors)

Prenatal Calcium and Vitamin D Intake, and Bone Mass in Later Life

Biomechanics (M Silva and P Zysset, Section Editors)

Ultrasound to Assess Bone Quality

Nutrition, Exercise, and Lifestyle in Osteoporosis (C Weaver and S Ferrari, Section Editors)

The Effects of Flavonoids on Bone