Top

Published in:

01-02-2021 | Osteoarthrosis | Review Article

Potential role of mitochondria in synoviocytes

Authors: Muzhe Li, Xuling Luo, Xin Long, Peishi Jiang, Qin Jiang, Heng Guo, Zhiwei Chen

Published in: Clinical Rheumatology | Issue 2/2021

Abstract

Synoviocytes are located in the synovium lining layer, which is composed of macrophage-like synoviocytes (MLS) and fibroblast-like synoviocytes (FLS) with different characteristics. Mitochondria, which exist in most cells, are two membrane-covered organelles. In addition to providing the necessary ATP for synoviocytes, mitochondria are involved in the regulation of redox homeostasis and the integration of synoviocytes death signals. In recent years, mitochondrial dysfunction has been found in rheumatoid arthritis (RA) and osteoarthritis (OA). Interestingly, recent studies have started uncovering that mitochondria that were previously reported to play a role in chondrocytes or immune cells, but not known to have pronounced roles in synoviocytes, can actually play crucial roles in the regulation of the pathological properties of the synoviocytes. The purpose of this review is to summarize our current understanding of the key role of mitochondria in synoviocytes, including mitochondrial dysfunction in synoviocytes can induce and aggravate inflammatory responses and changes in mitochondrial structure and function with the involvement of multiple cytokines, signal pathway, and hypoxic state of synovial tissue alter the response of synoviocytes to apoptotic stimulation. Also, mitochondrial abnormalities in synoviocytes promote the synoviocytes invasion and proliferation.

Mathiessen A, Conaghan PG (2017) Synovitis in osteoarthritis: current understanding with therapeutic implications. Arthritis Res Ther 19(1):18. https://doi.org/10.1186/s13075-017-1229-9CrossRefPubMedPubMedCentral

Bartok B, Firestein GS (2010) Fibroblast-like synoviocytes: key effector cells in rheumatoid arthritis. Immunol Rev 233(1):233–255. https://doi.org/10.1111/j.0105-2896.2009.00859.xCrossRefPubMedPubMedCentral

Chang SK, Gu Z, Brenner MB (2010) Fibroblast-like synoviocytes in inflammatory arthritis pathology: the emerging role of cadherin-11. Immunol Rev 233(1):256–266. https://doi.org/10.1111/j.0105-2896.2009.00854.xCrossRefPubMed

Tu J, Hong W, Zhang P, Wang X, Korner H, Wei W (2018) Ontology and function of fibroblast-like and macrophage-like synoviocytes: how do they talk to each other and can they be targeted for rheumatoid arthritis therapy? Front Immunol 9:1467. https://doi.org/10.3389/fimmu.2018.01467CrossRefPubMedPubMedCentral

Brennan FM, McInnes IB (2008) Evidence that cytokines play a role in rheumatoid arthritis. J Clin Invest 118(11):3537–3545. https://doi.org/10.1172/JCI36389CrossRefPubMedPubMedCentral

Muller-Ladner U, Ospelt C, Gay S, Distler O, Pap T (2007) Cells of the synovium in rheumatoid arthritis. Synovial fibroblasts. Arthritis Res Ther 9(6):223. https://doi.org/10.1186/ar2337CrossRefPubMedPubMedCentral

Martinou JC, Youle RJ (2011) Mitochondria in apoptosis: Bcl-2 family members and mitochondrial dynamics. Dev Cell 21(1):92–101. https://doi.org/10.1016/j.devcel.2011.06.017CrossRefPubMedPubMedCentral

Calvani R, Joseph AM, Adhihetty PJ, Miccheli A, Bossola M, Leeuwenburgh C, Bernabei R, Marzetti E (2013) Mitochondrial pathways in sarcopenia of aging and disuse muscle atrophy. Biol Chem 394(3):393–414. https://doi.org/10.1515/hsz-2012-0247CrossRefPubMedPubMedCentral

Phull AR, Nasir B, Haq IU, Kim SJ (2018) Oxidative stress, consequences and ROS mediated cellular signaling in rheumatoid arthritis. Chem Biol Interact 281:121–136. https://doi.org/10.1016/j.cbi.2017.12.024CrossRefPubMed

10.

Lunec J, Herbert K, Blount S, Griffiths HR, Emery P (1994) 8-Hydroxydeoxyguanosine. A marker of oxidative DNA damage in systemic lupus erythematosus. FEBS Lett 348(2):131–138. https://doi.org/10.1016/0014-5793(94)00583-4CrossRefPubMed

11.

Zhong H, Yin H (2015) Role of lipid peroxidation derived 4-hydroxynonenal (4-HNE) in cancer: focusing on mitochondria. Redox Biol 4:193–199. https://doi.org/10.1016/j.redox.2014.12.011CrossRefPubMed

12.

Nissanka N, Moraes CT (2018) Mitochondrial DNA damage and reactive oxygen species in neurodegenerative disease. FEBS Lett 592(5):728–742. https://doi.org/10.1002/1873-3468.12956CrossRefPubMedPubMedCentral

13.

Wang T, Wang G, Zhang Y, Zhang J, Cao W, Chen X (2019) Effect of lentivirus-mediated overexpression or silencing of MnSOD on apoptosis of resveratrol-treated fibroblast-like synoviocytes in rheumatoid arthritis. Eur J Pharmacol 844:65–72. https://doi.org/10.1016/j.ejphar.2018.12.001CrossRefPubMed

14.

Mitsunaga S, Hosomichi K, Okudaira Y, Nakaoka H, Suzuki Y, Kuwana M, Sato S, Kaneko Y, Homma Y, Oka A, Shiina T, Inoko H, Inoue I (2015) Aggregation of rare/low-frequency variants of the mitochondria respiratory chain-related proteins in rheumatoid arthritis patients. J Hum Genet 60(8):449–454. https://doi.org/10.1038/jhg.2015.50CrossRefPubMed

15.

Blanco FJ, Rego-Perez I (2018) Mitochondria and mitophagy: biosensors for cartilage degradation and osteoarthritis. Osteoarthr Cartil 26(8):989–991. https://doi.org/10.1016/j.joca.2018.05.018CrossRef

16.

Kowaltowski AJ, de Souza-Pinto NC, Castilho RF, Vercesi AE (2009) Mitochondria and reactive oxygen species. Free Radic Biol Med 47(4):333–343. https://doi.org/10.1016/j.freeradbiomed.2009.05.004CrossRefPubMed

17.

Droge W (2002) Free radicals in the physiological control of cell function. Physiol Rev 82(1):47–95. https://doi.org/10.1152/physrev.00018.2001CrossRefPubMed

18.

Balogh E, Veale DJ, McGarry T, Orr C, Szekanecz Z, Ng CT, Fearon U, Biniecka M (2018) Oxidative stress impairs energy metabolism in primary cells and synovial tissue of patients with rheumatoid arthritis. Arthritis Res Ther 20(1):95. https://doi.org/10.1186/s13075-018-1592-1CrossRefPubMedPubMedCentral

19.

Roemer FW, Guermazi A, Felson DT, Niu J, Nevitt MC, Crema MD, Lynch JA, Lewis CE, Torner J, Zhang Y (2011) Presence of MRI-detected joint effusion and synovitis increases the risk of cartilage loss in knees without osteoarthritis at 30-month follow-up: the MOST study. Ann Rheum Dis 70(10):1804–1809. https://doi.org/10.1136/ard.2011.150243CrossRefPubMedPubMedCentral

20.

Baker K, Grainger A, Niu J, Clancy M, Guermazi A, Crema M, Hughes L, Buckwalter J, Wooley A, Nevitt M, Felson DT (2010) Relation of synovitis to knee pain using contrast-enhanced MRIs. Ann Rheum Dis 69(10):1779–1783. https://doi.org/10.1136/ard.2009.121426CrossRefPubMed

21.

Meyer A, Laverny G, Bernardi L, Charles AL, Alsaleh G, Pottecher J, Sibilia J, Geny B (2018) Mitochondria: an organelle of bacterial origin controlling inflammation. Front Immunol 9:536. https://doi.org/10.3389/fimmu.2018.00536CrossRefPubMedPubMedCentral

22.

Collins LV, Hajizadeh S, Holme E, Jonsson IM, Tarkowski A (2004) Endogenously oxidized mitochondrial DNA induces in vivo and in vitro inflammatory responses. J Leukoc Biol 75(6):995–1000. https://doi.org/10.1189/jlb.0703328CrossRefPubMed

23.

Gu Y, Wang C, Roifman CM, Cohen A (2003) Role of MHC class I in immune surveillance of mitochondrial DNA integrity. J Immunol 170(7):3603–3607. https://doi.org/10.4049/jimmunol.170.7.3603CrossRefPubMed

24.

Ospelt C, Gay S (2005) Somatic mutations in mitochondria: the chicken or the egg? Arthritis Res Ther 7(5):179. https://doi.org/10.1186/ar1809CrossRefPubMedPubMedCentral

25.

Biniecka M, Fox E, Gao W, Ng CT, Veale DJ, Fearon U, O'Sullivan J (2011) Hypoxia induces mitochondrial mutagenesis and dysfunction in inflammatory arthritis. Arthritis Rheum 63(8):2172–2182. https://doi.org/10.1002/art.30395CrossRefPubMed

26.

Zhou R, Tardivel A, Thorens B, Choi I, Tschopp J (2010) Thioredoxin-interacting protein links oxidative stress to inflammasome activation. Nat Immunol 11(2):136–140. https://doi.org/10.1038/ni.1831CrossRefPubMed

27.

Fahmi H, He Y, Zhang M, Martel-Pelletier J, Pelletier JP, Di Battista JA (2001) Nimesulide reduces interleukin-1beta-induced cyclooxygenase-2 gene expression in human synovial fibroblasts. Osteoarthr Cartil 9(4):332–340. https://doi.org/10.1053/joca.2000.0393CrossRef

28.

Woo CH, Eom YW, Yoo MH, You HJ, Han HJ, Song WK, Yoo YJ, Chun JS, Kim JH (2000) Tumor necrosis factor-alpha generates reactive oxygen species via a cytosolic phospholipase A2-linked cascade. J Biol Chem 275(41):32357–32362. https://doi.org/10.1074/jbc.M005638200CrossRefPubMed

29.

Valcarcel-Ares MN, Riveiro-Naveira RR, Vaamonde-Garcia C, Loureiro J, Hermida-Carballo L, Blanco FJ, Lopez-Armada MJ (2014) Mitochondrial dysfunction promotes and aggravates the inflammatory response in normal human synoviocytes. Rheumatology (Oxford) 53(7):1332–1343. https://doi.org/10.1093/rheumatology/keu016CrossRef

30.

Vaamonde-Garcia C, Loureiro J, Valcarcel-Ares MN, Riveiro-Naveira RR, Ramil-Gomez O, Hermida-Carballo L, Centeno A, Meijide-Failde R, Blanco FJ, Lopez-Armada MJ (2017) The mitochondrial inhibitor oligomycin induces an inflammatory response in the rat knee joint. BMC Musculoskelet Disord 18(1):254. https://doi.org/10.1186/s12891-017-1621-2CrossRefPubMedPubMedCentral

31.

Al-Azab M, Qaed E, Ouyang X, Elkhider A, Walana W, Li H, Li W, Tang Y, Adlat S, Wei J, Wang B, Li X (2020) TL1A/TNFR2-mediated mitochondrial dysfunction of fibroblast-like synoviocytes increases inflammatory response in patients with rheumatoid arthritis via reactive oxygen species generation. FEBS J. https://doi.org/10.1111/febs.15181

32.

Bulua AC, Simon A, Maddipati R, Pelletier M, Park H, Kim KY, Sack MN, Kastner DL, Siegel RM (2011) Mitochondrial reactive oxygen species promote production of proinflammatory cytokines and are elevated in TNFR1-associated periodic syndrome (TRAPS). J Exp Med 208(3):519–533. https://doi.org/10.1084/jem.20102049CrossRefPubMedPubMedCentral

33.

Hu HL, Zhang ZX, Chen CS, Cai C, Zhao JP, Wang X (2010) Effects of mitochondrial potassium channel and membrane potential on hypoxic human pulmonary artery smooth muscle cells. Am J Respir Cell Mol Biol 42(6):661–666. https://doi.org/10.1165/rcmb.2009-0017OCCrossRefPubMed

34.

Shokolenko I, Venediktova N, Bochkareva A, Wilson GL, Alexeyev MF (2009) Oxidative stress induces degradation of mitochondrial DNA. Nucleic Acids Res 37(8):2539–2548. https://doi.org/10.1093/nar/gkp100CrossRefPubMedPubMedCentral

35.

Da Sylva TR, Connor A, Mburu Y, Keystone E, Wu GE (2005) Somatic mutations in the mitochondria of rheumatoid arthritis synoviocytes. Arthritis Res Ther 7(4):R844–R851. https://doi.org/10.1186/ar1752CrossRefPubMedPubMedCentral

36.

Harty LC, Biniecka M, O'Sullivan J, Fox E, Mulhall K, Veale DJ, Fearon U (2012) Mitochondrial mutagenesis correlates with the local inflammatory environment in arthritis. Ann Rheum Dis 71(4):582–588. https://doi.org/10.1136/annrheumdis-2011-200245CrossRefPubMed

37.

Biniecka M, Kennedy A, Ng CT, Chang TC, Balogh E, Fox E, Veale DJ, Fearon U, O'Sullivan JN (2011) Successful tumour necrosis factor (TNF) blocking therapy suppresses oxidative stress and hypoxia-induced mitochondrial mutagenesis in inflammatory arthritis. Arthritis Res Ther 13(4):R121. https://doi.org/10.1186/ar3424CrossRefPubMedPubMedCentral

38.

Eerola E, Pulkki K, Pelliniemi LJ, Vuorio E, Toivanen A (1988) Abnormal mitochondria in cultured synovial fibroblasts in rheumatoid and reactive arthritis? Br J Rheumatol 27(Suppl 2):128–131. https://doi.org/10.1093/rheumatology/xxvii.suppl_2.128CrossRefPubMed

39.

Pullerits R, Bokarewa M, Jonsson IM, Verdrengh M, Tarkowski A (2005) Extracellular cytochrome c, a mitochondrial apoptosis-related protein, induces arthritis. Rheumatology (Oxford) 44(1):32–39. https://doi.org/10.1093/rheumatology/keh406CrossRef

40.

Kim EK, Kwon JE, Lee SY, Lee EJ, Kim DS, Moon SJ, Lee J, Kwok SK, Park SH, Cho ML (2017) IL-17-mediated mitochondrial dysfunction impairs apoptosis in rheumatoid arthritis synovial fibroblasts through activation of autophagy. Cell Death Dis 8(1):e2565. https://doi.org/10.1038/cddis.2016.490CrossRefPubMedPubMedCentral

41.

Chipuk JE, Green DR (2008) How do BCL-2 proteins induce mitochondrial outer membrane permeabilization? Trends Cell Biol 18(4):157–164. https://doi.org/10.1016/j.tcb.2008.01.007CrossRefPubMedPubMedCentral

42.

Ola MS, Nawaz M, Ahsan H (2011) Role of Bcl-2 family proteins and caspases in the regulation of apoptosis. Mol Cell Biochem 351(1–2):41–58. https://doi.org/10.1007/s11010-010-0709-xCrossRefPubMed

43.

Busteed S, Bennett MW, Molloy C, Houston A, Stone MA, Shanahan F, Molloy MG, O'Connell J (2006) Bcl-x(L) expression in vivo in rheumatoid synovium. Clin Rheumatol 25(6):789–793. https://doi.org/10.1007/s10067-005-0191-0CrossRefPubMed

44.

Perlman H, Georganas C, Pagliari LJ, Koch AE, Haines K 3rd, Pope RM (2000) Bcl-2 expression in synovial fibroblasts is essential for maintaining mitochondrial homeostasis and cell viability. J Immunol 164(10):5227–5235. https://doi.org/10.4049/jimmunol.164.10.5227CrossRefPubMed

45.

Kurowska M, Rudnicka W, Kontny E, Janicka I, Chorazy M, Kowalczewski J, Ziolkowska M, Ferrari-Lacraz S, Strom TB, Maslinski W (2002) Fibroblast-like synoviocytes from rheumatoid arthritis patients express functional IL-15 receptor complex: endogenous IL-15 in autocrine fashion enhances cell proliferation and expression of Bcl-x(L) and Bcl-2. J Immunol 169(4):1760–1767. https://doi.org/10.4049/jimmunol.169.4.1760CrossRefPubMed

46.

Kim SK, Park KY, Yoon WC, Park SH, Park KK, Yoo DH, Choe JY (2011) Melittin enhances apoptosis through suppression of IL-6/sIL-6R complex-induced NF-kappaB and STAT3 activation and Bcl-2 expression for human fibroblast-like synoviocytes in rheumatoid arthritis. Joint Bone Spine 78(5):471–477. https://doi.org/10.1016/j.jbspin.2011.01.004CrossRefPubMed

47.

Wang CY, Mayo MW, Korneluk RG, Goeddel DV, Baldwin AS Jr (1998) NF-kappaB antiapoptosis: induction of TRAF1 and TRAF2 and c-IAP1 and c-IAP2 to suppress caspase-8 activation. Science 281(5383):1680–1683. https://doi.org/10.1126/science.281.5383.1680CrossRefPubMed

48.

Liu H, Pope RM (2003) The role of apoptosis in rheumatoid arthritis. Curr Opin Pharmacol 3(3):317–322. https://doi.org/10.1016/s1471-4892(03)00037-7CrossRefPubMed

49.

Kammouni W, Wong K, Ma G, Firestein GS, Gibson SB, El-Gabalawy HS (2007) Regulation of apoptosis in fibroblast-like synoviocytes by the hypoxia-induced Bcl-2 family member Bcl-2/adenovirus E1B 19-kd protein-interacting protein 3. Arthritis Rheum 56(9):2854–2863. https://doi.org/10.1002/art.22853CrossRefPubMed

50.

Muller-Ladner U, Kriegsmann J, Franklin BN, Matsumoto S, Geiler T, Gay RE, Gay S (1996) Synovial fibroblasts of patients with rheumatoid arthritis attach to and invade normal human cartilage when engrafted into SCID mice. Am J Pathol 149(5):1607–1615PubMedPubMedCentral

51.

Henrotin YE, Bruckner P, Pujol JP (2003) The role of reactive oxygen species in homeostasis and degradation of cartilage. Osteoarthr Cartil 11(10):747–755. https://doi.org/10.1016/s1063-4584(03)00150-xCrossRef

52.

Biniecka M, Canavan M, McGarry T, Gao W, McCormick J, Cregan S, Gallagher L, Smith T, Phelan JJ, Ryan J, O'Sullivan J, Ng CT, Veale DJ, Fearon U (2016) Dysregulated bioenergetics: a key regulator of joint inflammation. Ann Rheum Dis 75(12):2192–2200. https://doi.org/10.1136/annrheumdis-2015-208476CrossRefPubMedPubMedCentral

53.

Nguyen TH, Paluck SJ, McGahran AJ, Maynard HD (2015) Poly (vinyl sulfonate) facilitates bFGF-induced cell proliferation. Biomacromolecules 16(9):2684–2692. https://doi.org/10.1021/acs.biomac.5b00557CrossRefPubMedPubMedCentral

54.

Sparks JA (2019) Rheumatoid arthritis. Ann Intern Med 170(1):ITC1–ITC16. https://doi.org/10.7326/AITC201901010CrossRefPubMed

55.

Fearon U, Canavan M, Biniecka M, Veale DJ (2016) Hypoxia, mitochondrial dysfunction and synovial invasiveness in rheumatoid arthritis. Nat Rev Rheumatol 12(7):385–397. https://doi.org/10.1038/nrrheum.2016.69CrossRefPubMed

56.

Quinonez-Flores CM, Gonzalez-Chavez SA, Pacheco-Tena C (2016) Hypoxia and its implications in rheumatoid arthritis. J Biomed Sci 23(1):62. https://doi.org/10.1186/s12929-016-0281-0CrossRefPubMedPubMedCentral

57.

McGarry T, Biniecka M, Veale DJ, Fearon U (2018) Hypoxia, oxidative stress and inflammation. Free Radic Biol Med 125:15–24. https://doi.org/10.1016/j.freeradbiomed.2018.03.042CrossRefPubMed

58.

Karami J, Aslani S, Tahmasebi MN, Mousavi MJ, Sharafat Vaziri A, Jamshidi A, Farhadi E, Mahmoudi M (2019) Epigenetics in rheumatoid arthritis; fibroblast-like synoviocytes as an emerging paradigm in the pathogenesis of the disease. Immunol Cell Biol 98:171–186. https://doi.org/10.1111/imcb.12311CrossRef

59.

Chalan P, van den Berg A, Kroesen BJ, Brouwer L, Boots A (2015) Rheumatoid arthritis, immunosenescence and the hallmarks of aging. Curr Aging Sci 8(2):131–146. https://doi.org/10.2174/1874609808666150727110744CrossRefPubMedPubMedCentral

60.

Lee SY, Park SH, Lee SW, Lee SH, Son MK, Choi YH, Chung WT, Yoo YH (2014) Synoviocyte apoptosis may differentiate responder and non-responder patients to methotrexate treatment in rheumatoid arthritis. Arch Pharm Res 37(10):1286–1294. https://doi.org/10.1007/s12272-014-0365-xCrossRefPubMed

61.

Miesel R, Murphy MP, Kroger H (1996) Enhanced mitochondrial radical production in patients which rheumatoid arthritis correlates with elevated levels of tumor necrosis factor alpha in plasma. Free Radic Res 25(2):161–169. https://doi.org/10.3109/10715769609149921CrossRefPubMed

62.

Derambure C, Dzangue-Tchoupou G, Berard C, Vergne N, Hiron M, D'Agostino MA, Musette P, Vittecoq O, Lequerre T (2017) Pre-silencing of genes involved in the electron transport chain (ETC) pathway is associated with responsiveness to abatacept in rheumatoid arthritis. Arthritis Res Ther 19(1):109. https://doi.org/10.1186/s13075-017-1319-8CrossRefPubMedPubMedCentral

63.

McGarry T, Orr C, Wade S, Biniecka M, Wade S, Gallagher L, Low C, Veale DJ, Fearon U (2018) JAK/STAT blockade alters synovial bioenergetics, mitochondrial function, and proinflammatory mediators in rheumatoid arthritis. Arthritis Rheumatol 70(12):1959–1970. https://doi.org/10.1002/art.40569CrossRefPubMed

64.

Zhang Q, Liu J, Zhang M, Wei S, Li R, Gao Y, Peng W, Wu C (2019) Apoptosis induction of fibroblast-like synoviocytes is an important molecular-mechanism for herbal medicine along with its active components in treating rheumatoid arthritis. Biomolecules 9(12). https://doi.org/10.3390/biom9120795

65.

Abramoff B, Caldera FE (2020) Osteoarthritis: pathology, diagnosis, and treatment options. Med Clin North Am 104(2):293–311. https://doi.org/10.1016/j.mcna.2019.10.007CrossRefPubMed

66.

Wu L, Liu H, Li L, Liu H, Cheng Q, Li H, Huang H (2014) Mitochondrial pathology in osteoarthritic chondrocytes. Curr Drug Targets 15(7):710–719. https://doi.org/10.2174/1389450115666140417120305CrossRefPubMed

67.

Blanco FJ, Rego I, Ruiz-Romero C (2011) The role of mitochondria in osteoarthritis. Nat Rev Rheumatol 7(3):161–169. https://doi.org/10.1038/nrrheum.2010.213CrossRefPubMed

68.

Vaamonde-Garcia C, Riveiro-Naveira RR, Valcarcel-Ares MN, Hermida-Carballo L, Blanco FJ, Lopez-Armada MJ (2012) Mitochondrial dysfunction increases inflammatory responsiveness to cytokines in normal human chondrocytes. Arthritis Rheum 64(9):2927–2936. https://doi.org/10.1002/art.34508CrossRefPubMed

69.

Zhou S, Wen H, Cai W, Zhang Y, Li H (2019) Effect of hypoxia/reoxygenation on the biological effect of IGF system and the inflammatory mediators in cultured synoviocytes. Biochem Biophys Res Commun 508(1):17–24. https://doi.org/10.1016/j.bbrc.2018.11.099CrossRefPubMed

70.

Cillero-Pastor B, Martin MA, Arenas J, Lopez-Armada MJ, Blanco FJ (2011) Effect of nitric oxide on mitochondrial activity of human synovial cells. BMC Musculoskelet Disord 12:42. https://doi.org/10.1186/1471-2474-12-42CrossRefPubMedPubMedCentral

71.

Loeser RF, Collins JA, Diekman BO (2016) Ageing and the pathogenesis of osteoarthritis. Nat Rev Rheumatol 12(7):412–420. https://doi.org/10.1038/nrrheum.2016.65CrossRefPubMedPubMedCentral

72.

Chang MC, Hung SC, Chen WY, Chen TL, Lee CF, Lee HC, Wang KL, Chiou CC, Wei YH (2005) Accumulation of mitochondrial DNA with 4977-bp deletion in knee cartilage--an association with idiopathic osteoarthritis. Osteoarthr Cartil 13(11):1004–1011. https://doi.org/10.1016/j.joca.2005.06.011CrossRef

73.

Zhao Z, Li Y, Wang M, Jin Y, Liao W, Zhao Z, Fang J (2020) Mitochondrial DNA haplogroups participate in osteoarthritis: current evidence based on a meta-analysis. Clin Rheumatol 39:1027–1037. https://doi.org/10.1007/s10067-019-04890-xCrossRefPubMed

74.

Hsu HC, Chang WM, Wu JY, Huang CC, Lu FJ, Chuang YW, Chang PJ, Chen KH, Hong CZ, Yeh RH, Liu TZ, Chen CH (2016) Folate deficiency triggered apoptosis of synoviocytes: role of overproduction of reactive oxygen species generated via NADPH oxidase/mitochondrial complex II and calcium perturbation. PLoS One 11(1):e0146440. https://doi.org/10.1371/journal.pone.0146440CrossRefPubMedPubMedCentral

75.

Veale DJ, Fearon U (2018) The pathogenesis of psoriatic arthritis. Lancet 391(10136):2273–2284. https://doi.org/10.1016/S0140-6736(18)30830-4CrossRefPubMed

76.

Dalbeth N, Pool B, Smith T, Callon KE, Lobo M, Taylor WJ, Jones PB, Cornish J, McQueen FM (2010) Circulating mediators of bone remodeling in psoriatic arthritis: implications for disordered osteoclastogenesis and bone erosion. Arthritis Res Ther 12(4):R164. https://doi.org/10.1186/ar3123CrossRefPubMedPubMedCentral

77.

Chimenti MS, Sunzini F, Fiorucci L, Botti E, Fonti GL, Conigliaro P, Triggianese P, Costa L, Caso F, Giunta A, Esposito M, Bianchi L, Santucci R, Perricone R (2018) Potential role of cytochrome c and tryptase in psoriasis and psoriatic arthritis pathogenesis: focus on resistance to apoptosis and oxidative stress. Front Immunol 9:2363. https://doi.org/10.3389/fimmu.2018.02363CrossRefPubMedPubMedCentral

78.

Firuzi O, Spadaro A, Spadaro C, Riccieri V, Petrucci R, Marrosu G, Saso L (2008) Protein oxidation markers in the serum and synovial fluid of psoriatic arthritis patients. J Clin Lab Anal 22(3):210–215. https://doi.org/10.1002/jcla.20243CrossRefPubMedPubMedCentral

79.

Kumagai T, Matsukawa N, Kaneko Y, Kusumi Y, Mitsumata M, Uchida K (2004) A lipid peroxidation-derived inflammatory mediator: identification of 4-hydroxy-2-nonenal as a potential inducer of cyclooxygenase-2 in macrophages. J Biol Chem 279(46):48389–48396. https://doi.org/10.1074/jbc.M409935200CrossRefPubMed

80.

Coto-Segura P, Santos-Juanes J, Gomez J, Alvarez V, Diaz M, Alonso B, Corao AI, Coto E (2012) Common European mitochondrial haplogroups in the risk for psoriasis and psoriatic arthritis. Genet Test Mol Biomarkers 16(6):621–623. https://doi.org/10.1089/gtmb.2011.0266CrossRefPubMed

Title: Potential role of mitochondria in synoviocytes
Authors: Muzhe Li
Xuling Luo
Xin Long
Peishi Jiang
Qin Jiang
Heng Guo
Zhiwei Chen
Publication date: 01-02-2021
Publisher: Springer International Publishing
Keywords: Osteoarthrosis
Osteoarthrosis
Psoriatic Arthritis
Rheumatoid Arthritis
Cytokines
Published in: Clinical Rheumatology / Issue 2/2021
Print ISSN: 0770-3198
Electronic ISSN: 1434-9949
DOI: https://doi.org/10.1007/s10067-020-05263-5

ACC 2024 Congress Coverage

Heart Failure Video

At a glance: The ONWARDS insulin icodec trials

Springer Medicine

Potential role of mitochondria in synoviocytes

Abstract

ACC 2024 Congress Coverage

Year in Review: Heart failure and cardiomyopathies

Semaglutide benefits people with type 2 diabetes and obesity-related heart failure

Incentivised to exercise

New intervention for STEMI-related cardiogenic shock

» View more highlights on the ACC 2024 congress hub page

At a glance: The ONWARDS insulin icodec trials

Springer Medicine

Abstract

Please log in to get access to this content

Other articles of this Issue 2/2021

Response to: Caution the masqueraders of Good’s syndrome on the thymoma with systemic lupus erythematosus

Insights into the choice between intravenous infusion and subcutaneous injection: physician and patient characteristics driving treatment in SLE

Kidney transplantation as a treatment of choice for AA amyloidosis due to periodic fever syndrome

Comparison of efficacy and safety of urate-lowering therapies for hyperuricemic patients with gout: a meta-analysis of randomized, controlled trials

The multifaceted functional role of DNA methylation in immune-mediated rheumatic diseases

Dorsal root ganglia: fibromyalgia pain factory?

ACC 2024 Congress Coverage

Year in Review: Heart failure and cardiomyopathies

Semaglutide benefits people with type 2 diabetes and obesity-related heart failure

Incentivised to exercise

New intervention for STEMI-related cardiogenic shock

» View more highlights on the ACC 2024 congress hub page