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Journal of Zhejiang University SCIENCE B 2024 Vol.25 No.3 P.197-211

http://doi.org/10.1631/jzus.B2300402


Advances in the study of mitophagy in osteoarthritis


Author(s):  Hong CAO, Xuchang ZHOU, Bowen XU, Han HU, Jianming GUO, Miao WANG, Nan LI, Jun ZOU

Affiliation(s):  Department of Sport Rehabilitation, Shanghai University of Sport, Shanghai 200438, China; more

Corresponding email(s):   junzou@sus.edu.cn, linan@immunol.org

Key Words:  Mitophagy, Osteoarthritis, Chondrocyte, Mitochondria, Apoptosis


Hong CAO, Xuchang ZHOU, Bowen XU, Han HU, Jianming GUO, Miao WANG, Nan LI, Jun ZOU. Advances in the study of mitophagy in osteoarthritis[J]. Journal of Zhejiang University Science B, 2024, 25(3): 197-211.

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author="Hong CAO, Xuchang ZHOU, Bowen XU, Han HU, Jianming GUO, Miao WANG, Nan LI, Jun ZOU",
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doi="10.1631/jzus.B2300402"
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A1 - Miao WANG
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A1 - Jun ZOU
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Abstract: 
osteoarthritis (OA), characterized by cartilage degeneration, synovial inflammation, and subchondral bone remodeling, is among the most common musculoskeletal disorders globally in people over 60 years of age. The initiation and progression of OA involves the abnormal metabolism of chondrocytes as an important pathogenic process. Cartilage degeneration features mitochondrial dysfunction as one of the important causative factors of abnormal chondrocyte metabolism. Therefore, maintaining mitochondrial homeostasis is an important strategy to mitigate OA. mitophagy is a vital process for autophagosomes to target, engulf, and remove damaged and dysfunctional mitochondria, thereby maintaining mitochondrial homeostasis. Cumulative studies have revealed a strong association between mitophagy and OA, suggesting that the regulation of mitophagy may be a novel therapeutic direction for OA. By reviewing the literature on mitophagy and OA published in recent years, this paper elaborates the potential mechanism of mitophagy regulating OA, thus providing a theoretical basis for studies related to mitophagy to develop new treatment options for OA.

线粒体自噬调控骨关节炎的最新进展

曹红1,2,周绪昌1,3,徐博文2,胡涵2,郭健民1,王淼1,李楠2,邹军1
1上海体育大学运动健康学院,中国上海市,200438
2海军军医大学免疫与炎症全国重点实验室,中国上海市,200433
3北京体育大学运动医学与康复学院,中国北京市,100084
摘要:骨关节炎是一种以关节内软骨损伤退变、软骨下骨异常重塑、骨赘生成、滑膜炎症反应和广泛血管生成为特征的慢性退行性关节疾病,是全球60岁以上人群最常见的肌肉骨骼疾病。在骨关节炎的发生发展过程中,软骨细胞的异常代谢发挥了重要致病作用。线粒体功能障碍作为软骨细胞代谢异常的重要诱因,参与了骨关节炎的发生和发展。因此,维持线粒体稳态是一种避免骨关节炎发生的重要方式。线粒体自噬是自噬体靶向吞噬损伤线粒体,以清除受损或功能失调的线粒体,维持线粒体稳态的一种方式。越来越多的研究发现线粒体自噬与骨关节炎密切相关,这提示线粒体自噬功能的调节可以作为一种治疗骨关节炎的新方法。本文通过对近年来线粒体自噬在骨关节炎中的研究进行综述,进一步阐述了线粒体自噬调控骨关节炎的潜在机制,为线粒体自噬治疗骨关节炎的相关研究提供理论依据。

关键词:线粒体自噬;骨关节炎;软骨细胞;线粒体;凋亡

Darkslateblue:Affiliate; Royal Blue:Author; Turquoise:Article

Reference

[1]AkasakiY, Alvarez-GarciaO, SaitoM, et al., 2014. FoxO transcription factors support oxidative stress resistance in human chondrocytes. Arthritis Rheumatol, 66(12):3349-3358.

[2]Almonte-BecerrilM, Navarro-GarciaF, Gonzalez-RoblesA, et al., 2010. Cell death of chondrocytes is a combination between apoptosis and autophagy during the pathogenesis of osteoarthritis within an experimental model. Apoptosis, 15(5):631-638.

[3]AndingAL, BaehreckeEH, 2017. Cleaning house: selective autophagy of organelles. Dev Cell, 41(1):10-22.

[4]AnsariMY, KhanNM, AhmadI, et al., 2018. Parkin clearance of dysfunctional mitochondria regulates ROS levels and increases survival of human chondrocytes. Osteoarthritis Cartilage, 26(8):1087-1097.

[5]AnsariMY, AhmadN, HaqqiTM, 2020. Oxidative stress and inflammation in osteoarthritis pathogenesis: role of polyphenols. Biomed Pharmacother, 129:110452.

[6]ArraM, SwarnkarG, KeK, et al., 2020. LDHA-mediated ROS generation in chondrocytes is a potential therapeutic target for osteoarthritis. Nat Commun, 11:3427.

[7]BellotG, Garcia-MedinaR, GounonP, et al., 2009. Hypoxia-induced autophagy is mediated through hypoxia-inducible factor induction of BNIP3 and BNIP3L via their BH3 domains. Mol Cell Biol, 29(10):2570-2581.

[8]BernardiniJP, BrouwerJM, TanIKL, et al., 2019. Parkin inhibits BAK and BAX apoptotic function by distinct mechanisms during mitophagy. EMBO J, 38(2):e99916.

[9]BhujabalZ, BirgisdottirÅB, SjøttemE, et al., 2017. FKBP8 recruits LC3A to mediate parkin-independent mitophagy. EMBO Rep, 18(6):947-961.

[10]BingolB, TeaJS, PhuL, et al., 2014. The mitochondrial deubiquitinase USP30 opposes parkin-mediated mitophagy. Nature, 510(7505):370-375.

[11]BirgisdottirÅB, MouilleronS, BhujabalZ, et al., 2019. Members of the autophagy class III phosphatidylinositol 3-kinase complex I interact with GABARAP and GABARAPL1 via LIR motifs. Autophagy, 15(8):1333-1355.

[12]BlancoFJ, Rego-PérezI, 2018. Mitochondria and mitophagy: biosensors for cartilage degradation and osteoarthritis. Osteoarthritis Cartilage, 26(8):989-991.

[13]BlancoFJ, RegoI, Ruiz-RomeroC, 2011. The role of mitochondria in osteoarthritis. Nat Rev Rheumatol, 7(3):161-169.

[14]BuluaAC, SimonA, MaddipatiR, et al., 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.

[15]CaoST, WangCC, YanJT, et al., 2020. Curcumin ameliorates oxidative stress-induced intestinal barrier injury and mitochondrial damage by promoting Parkin dependent mitophagy through AMPK-TFEB signal pathway. Free Radical Biol Med, 147:8-22.

[16]CharlierE, DeroyerC, CiregiaF, et al., 2019. Chondrocyte dedifferentiation and osteoarthritis (OA). Biochem Pharmacol, 165:49-65.

[17]ChenG, HanZ, FengD, et al., 2014. A regulatory signaling loop comprising the PGAM5 phosphatase and CK2 controls receptor-mediated mitophagy. Mol Cell, 54(3):362-377.

[18]ChenM, ChenZH, WangYY, et al., 2016. Mitophagy receptor FUNDC1 regulates mitochondrial dynamics and mitophagy. Autophagy, 12(4):689-702.

[19]CheongH, NairU, GengJF, et al., 2008. The Atg1 kinase complex is involved in the regulation of protein recruitment to initiate sequestering vesicle formation for nonspecific autophagy in Saccharomyces cerevisiae. Mol Biol Cell, 19(2):668-681.

[20]CollinsJA, WoodST, NelsonKJ, et al., 2016. Oxidative stress promotes peroxiredoxin hyperoxidation and attenuates pro-survival signaling in aging chondrocytes. J Biol Chem, 291(13):6641-6654.

[21]CoryellPR, DiekmanBO, LoeserRF, 2021. Mechanisms and therapeutic implications of cellular senescence in osteoarthritis. Nat Rev Rheumatol, 17(1):47-57.

[22]CuervoAM, BergaminiE, BrunkUT, et al., 2005. Autophagy and aging: the importance of maintaining “clean” cells. Autophagy, 1(3):131-140.

[23]CuiAY, LiHZ, WangDW, et al., 2020. Global, regional prevalence, incidence and risk factors of knee osteoarthritis in population-based studies. EClinicalMedicine, 29:100587.

[24]D'AdamoS, CetrulloS, GuidottiS, et al., 2020. Spermidine rescues the deregulated autophagic response to oxidative stress of osteoarthritic chondrocytes. Free Radic Biol Med, 153:159-172.

[25]DaiSH, ChenT, WangYH, et al., 2014. Sirt3 protects cortical neurons against oxidative stress via regulating mitochondrial Ca2+ and mitochondrial biogenesis. Int J Mol Sci, 15(8):14591-14609.

[26]D'AmicoD, OlmerM, FouassierAM, et al., 2022. Urolithin A improves mitochondrial health, reduces cartilage degeneration, and alleviates pain in osteoarthritis. Aging Cell, 21(8):e13662.

[27]DavisJE, PriceLL, LoGH, et al., 2017. A single recent injury is a potent risk factor for the development of accelerated knee osteoarthritis: data from the osteoarthritis initiative. Rheumatol Int, 37(10):1759-1764.

[28]DawsonTM, DawsonVL, 2017. Mitochondrial mechanisms of neuronal cell death: potential therapeutics. Annu Rev Pharmacol Toxicol, 57:437-454.

[29]DengR, WangY, BuYH, et al., 2022. BNIP3 mediates the different adaptive responses of fibroblast-like synovial cells to hypoxia in patients with osteoarthritis and rheumatoid arthritis. Mol Med, 28:64.

[30]DuanR, XieH, LiuZZ, 2020. The role of autophagy in osteoarthritis. Front Cell Dev Biol, 8:608388.

[31]DuanYM, FangHB, 2016. RecQL4 regulates autophagy and apoptosis in U2OS cells. Biochem Cell Biol, 94(6):551-559.

[32]EdgarRS, GreenEW, ZhaoYW, et al., 2012. Peroxiredoxins are conserved markers of circadian rhythms. Nature, 485(7399):459-464.

[33]EganDF, ShackelfordDB, MihaylovaMM, et al., 2011. Phosphorylation of ULK1 (hATG1) by AMP-activated protein kinase connects energy sensing to mitophagy. Science, 331(6016):456-461.

[34]EyreD, 2002. Articular cartilage and changes in Arthritis: collagen of articular cartilage. Arthritis Res Ther, 4:30.

[35]FengXF, PanJY, LiJY, et al., 2020. Metformin attenuates cartilage degeneration in an experimental osteoarthritis model by regulating AMPK/mTOR. Aging (Albany NY), 12(2):1087-1103.

[36]Fernández-MorenoM, Rego-PérezI, BlancoFJ, 2022. Is osteoarthritis a mitochondrial disease? What is the evidence? Curr Opin Rheumatol, 34(1):46-53.

[37]FivensonEM, LautrupS, SunN, et al., 2017. Mitophagy in neurodegeneration and aging. Neurochem Int, 109:202-209.

[38]FriedmanJR, NunnariJ, 2014. Mitochondrial form and function. Nature, 505(7483):335-343.

[39]FuruyaN, KakutaS, SumiyoshiK, et al., 2018. NDP52 interacts with mitochondrial RNA poly(A) polymerase to promote mitophagy. EMBO Rep, 19(12):e46363.

[40]GlickD, BarthS, MacleodKF, 2010. Autophagy: cellular and molecular mechanisms. J Pathol, 221(1):3-12.

[41]Glyn-JonesS, PalmerAJR, AgricolaR, et al., 2015. Osteoarthritis. Lancet, 386(9991):376-387.

[42]HannaRA, QuinsayMN, OrogoAM, et al., 2012. Microtubule-associated protein 1 light chain 3 (LC3) interacts with Bnip3 protein to selectively remove endoplasmic reticulum and mitochondria via autophagy. J Biol Chem, 287(23):19094-19104.

[43]HardieDG, 2014. AMP-activated protein kinase: maintaining energy homeostasis at the cellular and whole-body levels. Annu Rev Nutr, 34:31-55.

[44]HeJ, HeJ, 2023. Baicalin mitigated IL-1β-induced osteoarthritis chondrocytes damage through activating mitophagy. Chem Biol Drug Des, 101(6):1322-1334.

[45]HeYZ, WuZP, XuLH, et al., 2020. The role of SIRT3-mediated mitochondrial homeostasis in osteoarthritis. Cell Mol Life Sci, 77(19):3729-3743.

[46]HerzigS, ShawRJ, 2018. AMPK: guardian of metabolism and mitochondrial homeostasis. Nat Rev Mol Cell Biol, 19(2):121-135.

[47]Higuchi-SanabriaR, FrankinoPA, PaulJW III, et al., 2018. A futile battle? Protein quality control and the stress of aging. Dev Cell, 44(2):139-163.

[48]HuSL, ZhangCW, NiLB, et al., 2020. Stabilization of HIF-1α alleviates osteoarthritis via enhancing mitophagy. Cell Death Dis, 11(6):481.

[49]HuangLW, HuangTC, HuYC, et al., 2020. Zinc protects chondrocytes from monosodium iodoacetate-induced damage by enhancing ATP and mitophagy. Biochem Biophys Res Commun, 521(1):50-56.

[50]HunterW, 1995. Of the structure and disease of articulating cartilages. Clin Orthop Relat Res, (317):3-6.

[51]IbrahimBA, AlenaziFSH, BriskiKP, 2015. Energy status determines hindbrain signal transduction pathway transcriptional reactivity to AMPK in the estradiol-treated ovariectomized female rat. Neuroscience, 284:888-899.

[52]ImhofH, SulzbacherI, GramppS, et al., 2000. Subchondral bone and cartilage disease: a rediscovered functional unit. Invest Radiol, 35(10):581-588.

[53]JiangN, XingBZ, PengR, et al., 2022. Inhibition of Cpt1a alleviates oxidative stress-induced chondrocyte senescence via regulating mitochondrial dysfunction and activating mitophagy. Mech Ageing Dev, 205:111688.

[54]JinZZ, ChangBH, WeiYL, et al., 2022. Curcumin exerts chondroprotective effects against osteoarthritis by promoting AMPK/PINK1/Parkin-mediated mitophagy. Biomed Pharmacother, 151:113092.

[55]JonesDP, 2015. Redox theory of aging. Redox Biol, 5:71-79.

[56]KawamataT, KamadaY, KabeyaY, et al., 2008. Organization of the pre-autophagosomal structure responsible for autophagosome formation. Mol Biol Cell, 19(5):2039-2050.

[57]KerrJS, AdriaanseBA, GreigNH, et al., 2017. Mitophagy and Alzheimer’s disease: cellular and molecular mechanisms. Trends Neurosci, 40(3):151-166.

[58]KiaerT, GrønlundJ, SørensenKH, 1988. Subchondral pO2, pCO2, pressure, pH, and lactate in human osteoarthritis of the hip. Clin Orthop Relat Res, (229):149-155.

[59]KianiC, ChenLW, WuYJ, et al., 2002. Structure and function of aggrecan. Cell Res, 12(1):19-32.

[60]KimC, NevittM, GuermaziA, et al., 2018. Brief report: leg length inequality and hip osteoarthritis in the multicenter osteoarthritis study and the osteoarthritis initiative. Arthritis Rheumatol, 70(10):1572-1576.

[61]KimD, SongJ, JinEJ, 2021. BNIP3-dependent mitophagy via PGC1α promotes cartilage degradation. Cells, 10(7):1839.

[62]KimHA, SuhDI, SongYW, 2001. Relationship between chondrocyte apoptosis and matrix depletion in human articular cartilage. J Rheumatol, 28(9):2038-2045.

[63]KimuraS, NodaT, YoshimoriT, 2008. Dynein-dependent movement of autophagosomes mediates efficient encounters with lysosomes. Cell Struct Funct, 33(1):109-122.

[64]Kop'evaTN, Bel'skaiaOB, AstapenkoMG, et al., 1986. Morphology of articular cartilage in osteoarthrosis. Arkh Patol, 48(12):40-46 (in Russian).

[65]KoyanoF, OkatsuK, KosakoH, et al., 2014. Ubiquitin is phosphorylated by PINK1 to activate parkin. Nature, 510(7503):162-166.

[66]LazarouM, SliterDA, KaneLA, et al., 2015. The ubiquitin kinase PINK1 recruits autophagy receptors to induce mitophagy. Nature, 524(7565):309-314.

[67]LeiQY, TanJ, YiSQ, et al., 2018. Mitochonic acid 5 activates the MAPK‒ERK‒yap signaling pathways to protect mouse microglial BV-2 cells against TNFα-induced apoptosis via increased Bnip3-related mitophagy. Cell Mol Biol Lett, 23:14.

[68]LiuD, CaiZJ, YangYT, et al., 2022. Mitochondrial quality control in cartilage damage and osteoarthritis: new insights and potential therapeutic targets. Osteoarthritis Cartilage, 30(3):395-405.

[69]LiuL, FengD, ChenG, et al., 2012. Mitochondrial outer-membrane protein FUNDC1 mediates hypoxia-induced mitophagy in mammalian cells. Nat Cell Biol, 14(2):177-185.

[70]LiuL, ZhangWY, LiuTH, et al., 2023. The physiological metabolite α-ketoglutarate ameliorates osteoarthritis by regulating mitophagy and oxidative stress. Redox Biol, 62:102663.

[71]LombardDB, AltFW, ChengHL, et al., 2007. Mammalian Sir2 homolog SIRT3 regulates global mitochondrial lysine acetylation. Mol Cell Biol, 27(24):8807-8814.

[72]LuJR, PengY, ZouJP, et al., 2021. Hypoxia inducible factor-1α is a regulator of autophagy in osteoarthritic chondrocytes. Cartilage, 13(2_suppl):1030s-1040s.

[73]MaZT, WangDL, WengJ, et al., 2020. BNIP3 decreases the LPS-induced inflammation and apoptosis of chondrocytes by promoting the development of autophagy. J Orthop Surg Res, 15:284.

[74]MaimaitijumaT, YuJH, RenYL, et al., 2020. PHF23 negatively regulates the autophagy of chondrocytes in osteoarthritis. Life Sci, 253:117750.

[75]MatsuhashiT, SatoT, KannoSI, et al., 2017. Mitochonic acid 5 (MA-5) facilitates ATP synthase oligomerization and cell survival in various mitochondrial diseases. eBioMedicine, 20:27-38.

[76]MeiRH, LouP, YouGC, et al., 2021. 17β-Estradiol induces mitophagy upregulation to protect chondrocytes via the SIRT1-mediated AMPK/mTOR signaling pathway. Front Endocrinol (Lausanne), 11:615250.

[77]MiwaS, KashyapS, ChiniE, et al., 2022. Mitochondrial dysfunction in cell senescence and aging. J Clin Invest, 132(13):e158447.

[78]NajafipourH, FerrellWR, 1995. Comparison of synovial PO2 and sympathetic vasoconstrictor responses in normal and acutely inflamed rabbit knee joints. Exp Physiol, 80(2):209-220.

[79]NguyenTN, PadmanBS, LazarouM, 2016. Deciphering the molecular signals of PINK1/Parkin mitophagy. Trends Cell Biol, 26(10):733-744.

[80]NovakI, KirkinV, McEwanDG, et al., 2010. Nix is a selective autophagy receptor for mitochondrial clearance. EMBO Rep, 11(1):45-51.

[81]PaulssonM, HeinegårdD, 1979. Matrix proteins bound to associatively prepared proteoglycans from bovine cartilage. Biochem J, 183(3):539-545.

[82]PedroJMBS, KroemerG, GalluzziL, 2017. Autophagy and mitophagy in cardiovascular disease. Circ Res, 120(11):1812-1824.

[83]PeturssonF, HusaM, JuneR, et al., 2013. Linked decreases in liver kinase B1 and AMP-activated protein kinase activity modulate matrix catabolic responses to biomechanical injury in chondrocytes. Arthritis Res Ther, 15(4):R77.

[84]PfanderD, GelseK, 2007. Hypoxia and osteoarthritis: how chondrocytes survive hypoxic environments. Curr Opin Rheumatol, 19(5):457-462.

[85]QinN, WeiLW, LiWY, et al., 2017. Local intra-articular injection of resveratrol delays cartilage degeneration in C57BL/6 mice by inducing autophagy via AMPK/mTOR pathway. J Pharmacol Sci, 134(3):166-174.

[86]ReedKN, WilsonG, PearsallA, et al., 2014. The role of mitochondrial reactive oxygen species in cartilage matrix destruction. Mol Cell Biochem, 397(1-2):195-201.

[87]RussellEM, MillerRH, UmbergerBR, et al., 2013. Lateral wedges alter mediolateral load distributions at the knee joint in obese individuals. J Orthop Res, 31(5):665-671.

[88]SalucciS, FalcieriE, BattistelliM, 2022. Chondrocyte death involvement in osteoarthritis. Cell Tissue Res, 389(2):159-170.

[89]SarrafSA, RamanM, Guarani-PereiraV, et al., 2013. Landscape of the PARKIN-dependent ubiquitylome in response to mitochondrial depolarization. Nature, 496(7445):372-376.

[90]Scherz-ShouvalR, ShvetsE, FassE, et al., 2007. Reactive oxygen species are essential for autophagy and specifically regulate the activity of Atg4. EMBO J, 26(7):1749-1760.

[91]SchulzRM, BaderA, 2007. Cartilage tissue engineering and bioreactor systems for the cultivation and stimulation of chondrocytes. Eur Biophys J, 36(4-5):539-568.

[92]ShangJ, LinN, PengR, et al., 2023. Inhibition of Klf10 attenuates oxidative stress-induced senescence of chondrocytes via modulating mitophagy. Molecules, 28(3):924.

[93]ShinHJ, ParkH, ShinN, et al., 2019. Pink1-mediated chondrocytic mitophagy contributes to cartilage degeneration in osteoarthritis. J Clin Med, 8(11):1849.

[94]SowterHM, RatcliffePJ, WatsonP, et al., 2001. HIF-1-dependent regulation of hypoxic induction of the cell death factors BNIP3 and NIX in human tumors. Cancer Res, 61(18):6669-6673.

[95]StolzA, ErnstA, DikicI, 2014. Cargo recognition and trafficking in selective autophagy. Nat Cell Biol, 16(6):495-501.

[96]SunK, JingXZ, GuoJC, et al., 2021. Mitophagy in degenerative joint diseases. Autophagy, 17(9):2082-2092.

[97]SuzukiK, KirisakoT, KamadaY, et al., 2001. The pre-autophagosomal structure organized by concerted functions of APG genes is essential for autophagosome formation. EMBO J, 20(21):5971-5981.

[98]SuzukiK, AkiokaM, Kondo-KakutaC, et al., 2013. Fine mapping of autophagy-related proteins during autophagosome formation in Saccharomyces cerevisiae. J Cell Sci, 126(Pt 11):2534-2544.

[99]TahrirFG, LangfordD, AminiS, et al., 2019. Mitochondrial quality control in cardiac cells: mechanisms and role in cardiac cell injury and disease. J Cell Physiol, 234(6):8122-8133.

[100]TamrakarP, IbrahimBA, GujarAD, et al., 2015. Estrogen regulates energy metabolic pathway and upstream adenosine 5'-monophosphate-activated protein kinase and phosphatase enzyme expression in dorsal vagal complex metabolosensory neurons during glucostasis and hypoglycemia. J Neurosci Res, 93(2):321-332.

[101]TangQ, ZhengG, FengZH, et al., 2017. Trehalose ameliorates oxidative stress-mediated mitochondrial dysfunction and ER stress via selective autophagy stimulation and autophagic flux restoration in osteoarthritis development. Cell Death Dis, 8(10):e3081.

[102]TianWL, LiW, ChenYQ, et al., 2015. Phosphorylation of ULK1 by AMPK regulates translocation of ULK1 to mitochondria and mitophagy. FEBS Lett, 589(15):1847-1854.

[103]VadalàG, di GiacomoG, AmbrosioL, et al., 2020. Irisin recovers osteoarthritic chondrocytes in vitro. Cells, 9(6):1478.

[104]VinaER, KwohCK, 2018. Epidemiology of osteoarthritis: literature update. Curr Opin Rheumatol, 30(2):160-167.

[105]WangCZ, YangY, ZhangYQ, et al., 2018. Protective effects of metformin against osteoarthritis through upregulation of SIRT3-mediated PINK1/Parkin-dependent mitophagy in primary chondrocytes. BioSci Trends, 12(6):605-612.

[106]WangFS, KuoCW, KoJY, et al., 2020. Irisin mitigates oxidative stress, chondrocyte dysfunction and osteoarthritis development through regulating mitochondrial integrity and autophagy. Antioxidants (Basel), 9(9):810.

[107]WangJL, WangK, HuangCA, et al., 2018. SIRT3 activation by dihydromyricetin suppresses chondrocytes degeneration via maintaining mitochondrial homeostasis. Int J Biol Sci, 14(13):1873-1882.

[108]WangS, DengZT, MaYC, et al., 2020. The role of autophagy and mitophagy in bone metabolic disorders. Int J Biol Sci, 16(14):2675-2691.

[109]WangWF, LiuSY, QiZF, et al., 2020. MiR-145 targeting BNIP3 reduces apoptosis of chondrocytes in osteoarthritis through notch signaling pathway. Eur Rev Med Pharmacol Sci, 24(16):8263-8272.

[110]WangYQ, SerricchioM, JaureguiM, et al., 2015. Deubiquitinating enzymes regulate PARK2-mediated mitophagy. Autophagy, 11(4):595-606.

[111]WilliamsJA, ZhaoK, JinSK, et al., 2017. New methods for monitoring mitochondrial biogenesis and mitophagy in vitro and in vivo. Exp Biol Med (Maywood), 242(8):781-787.

[112]WuLH, LiuHQ, LiLF, et al., 2014. Mitochondrial pathology in osteoarthritic chondrocytes. Curr Drug Targets, 15(7):710-719.

[113]WuWX, TianWL, HuZ, et al., 2014. ULK1 translocates to mitochondria and phosphorylates FUNDC1 to regulate mitophagy. EMBO Rep, 15(5):566-575.

[114]XianHX, WatariK, Sanchez-LopezE, et al., 2022. Oxidized DNA fragments exit mitochondria via mPTP- and VDAC-dependent channels to activate NLRP3 inflammasome and interferon signaling. Immunity, 55(8):1370-1385.e8.

[115]XinRB, XuYY, LongDB, et al., 2022. Mitochonic acid-5 inhibits reactive oxygen species production and improves human chondrocyte survival by upregulating SIRT3-mediated, Parkin-dependent mitophagy. Front Pharmacol, 13:911716.

[116]XuL, WuZ, HeY, et al., 2020. MFN2 contributes to metabolic disorders and inflammation in the aging of rat chondrocytes and osteoarthritis. Osteoarthritis Cartilage, 28(8):1079-1091.

[117]XuWN, YangRZ, ZhengHL, et al., 2019. PGC-1α acts as an mediator of Sirtuin2 to protect annulus fibrosus from apoptosis induced by oxidative stress through restraining mitophagy. Int J Biol Macromol, 136:1007-1017.

[118]YamamotoH, FujiokaY, SuzukiSW, et al., 2016. The intrinsically disordered protein Atg13 mediates supramolecular assembly of autophagy initiation complexes. Dev Cell, 38(1):86-99.

[119]YuWJ, GaoBL, LiN, et al., 2017. Sirt3 deficiency exacerbates diabetic cardiac dysfunction: role of Foxo3A-Parkin-mediated mitophagy. Biochim Biophys Acta (BBA)-Mol Basis Dis, 1863(8):1973-1983.

[120]YuXB, ChenGY, ZhouL, et al., 2022. Chondroprotective effects of Gubitong recipe via inhibiting excessive mitophagy of chondrocytes. Evid Based Complement Alternat Med, 2022:8922021.

[121]ZhangXJ, ChenS, SongL, et al., 2014. MTOR-independent, autophagic enhancer trehalose prolongs motor neuron survival and ameliorates the autophagic flux defect in a mouse model of amyotrophic lateral sclerosis. Autophagy, 10(4):588-602.

[122]ZhangYJ, LiuY, HouMZ, et al., 2023. Reprogramming of mitochondrial respiratory chain complex by targeting SIRT3-COX4I2 axis attenuates osteoarthritis progression. Adv Sci (Weinh), 10(10):2206144.

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