Advances in the study of mitophagy in osteoarthritis

Hong CAO; Xuchang ZHOU; Bowen XU; Han HU; Jianming GUO; Miao WANG; Nan LI; Jun ZOU

doi:10.1631/jzus.B2300402

Your Location：

Home >

Browse articles >

Advances in the study of mitophagy in osteoarthritis

Scan for full text

Alert me when the article has been cited

Submit

Review | Updated：2024-03-06

Advances in the study of mitophagy in osteoarthritis
Advances in the study of mitophagy in osteoarthritis
线粒体自噬调控骨关节炎的最新进展
Journal of Zhejiang University-SCIENCE B (Biomedicine & Biotechnology) Vol. 25, Issue 3, Pages: 197-211(2024)
Affiliations：

1.Department of Sport Rehabilitation, Shanghai University of Sport, Shanghai 200438, China
2.National Key Laboratory of Immunity and Inflammation, Naval Medical University, Shanghai 200433, China
3.School of Sport Medicine and Rehabilitation, Beijing Sport University, Beijing 100084, China
Funds：
DOI：10.1631/jzus.B2300402
CLC：
CSTR：

曹红,周绪昌,徐博文等.线粒体自噬调控骨关节炎的最新进展[J].浙江大学学报（英文版）（B辑：生物医学和生物技术）,2024,25(03):197-211.

Hong CAO, Xuchang ZHOU, Bowen XU, et al. Advances in the study of mitophagy in osteoarthritis. [J]. Journal of Zhejiang University-SCIENCE B (Biomedicine & Biotechnology) 25(3):197-211(2024)
曹红,周绪昌,徐博文等.线粒体自噬调控骨关节炎的最新进展[J].浙江大学学报（英文版）（B辑：生物医学和生物技术）,2024,25(03):197-211. DOI： 10.1631/jzus.B2300402.

Hong CAO, Xuchang ZHOU, Bowen XU, et al. Advances in the study of mitophagy in osteoarthritis. [J]. Journal of Zhejiang University-SCIENCE B (Biomedicine & Biotechnology) 25(3):197-211(2024) DOI： 10.1631/jzus.B2300402.

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。

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.

关键词

线粒体自噬骨关节炎软骨细胞线粒体凋亡

Keywords

MitophagyOsteoarthritisChondrocyteMitochondriaApoptosis

references

Akasaki Y, Alvarez-Garcia O, Saito M, et al., 2014. FoxO transcription factors support oxidative stress resistance in human chondrocytes. Arthritis Rheumatol, 66(12):3349-3358. https://doi.org/10.1002/art.38868https://doi.org/10.1002/art.38868

Almonte-Becerril M, Navarro-Garcia F, Gonzalez-Robles A, 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. https://doi.org/10.1007/s10495-010-0458-zhttps://doi.org/10.1007/s10495-010-0458-z

Anding AL, Baehrecke EH, 2017. Cleaning house: selective autophagy of organelles. Dev Cell, 41(1):10-22. https://doi.org/10.1016/j.devcel.2017.02.016https://doi.org/10.1016/j.devcel.2017.02.016

Ansari MY, Khan NM, Ahmad I, et al., 2018. Parkin clearance of dysfunctional mitochondria regulates ROS levels and increases survival of human chondrocytes. Osteoarthritis Cartilage, 26(8):1087-1097. https://doi.org/10.1016/j.joca.2017.07.020https://doi.org/10.1016/j.joca.2017.07.020

Ansari MY, Ahmad N, Haqqi TM, 2020. Oxidative stress and inflammation in osteoarthritis pathogenesis: role of polyphenols. Biomed Pharmacother, 129:110452. https://doi.org/10.1016/j.biopha.2020.110452https://doi.org/10.1016/j.biopha.2020.110452

Arra M, Swarnkar G, Ke K, et al., 2020. LDHA-mediated ROS generation in chondrocytes is a potential therapeutic target for osteoarthritis. Nat Commun, 11:3427. https://doi.org/10.1038/s41467-020-17242-0https://doi.org/10.1038/s41467-020-17242-0

Bellot G, Garcia-Medina R, Gounon P, 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. https://doi.org/10.1128/mcb.00166-09https://doi.org/10.1128/mcb.00166-09

Bernardini JP, Brouwer JM, Tan IKL, et al., 2019. Parkin inhibits BAK and BAX apoptotic function by distinct mechanisms during mitophagy. EMBO J, 38(2):e99916. https://doi.org/10.15252/embj.201899916https://doi.org/10.15252/embj.201899916

Bhujabal Z, Birgisdottir ÅB, Sjøttem E, et al., 2017. FKBP8 recruits LC3A to mediate parkin-independent mitophagy. EMBO Rep, 18(6):947-961. https://doi.org/10.15252/embr.201643147https://doi.org/10.15252/embr.201643147

Bingol B, Tea JS, Phu L, et al., 2014. The mitochondrial deubiquitinase USP30 opposes parkin-mediated mitophagy. Nature, 510(7505):370-375. https://doi.org/10.1038/nature13418https://doi.org/10.1038/nature13418

Birgisdottir ÅB, Mouilleron S, Bhujabal Z, 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. https://doi.org/10.1080/15548627.2019.1581009https://doi.org/10.1080/15548627.2019.1581009

Blanco FJ, Rego-Pérez I, 2018. Mitochondria and mitophagy: biosensors for cartilage degradation and osteoarthritis. Osteoarthritis Cartilage, 26(8):989-991. https://doi.org/10.1016/j.joca.2018.05.018https://doi.org/10.1016/j.joca.2018.05.018

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.2010.213https://doi.org/10.1038/nrrheum.2010.213

Bulua AC, Simon A, Maddipati R, 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. https://doi.org/10.1084/jem.20102049https://doi.org/10.1084/jem.20102049

Cao ST, Wang CC, Yan JT, 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. https://doi.org/10.1016/j.freeradbiomed.2019.12.004https://doi.org/10.1016/j.freeradbiomed.2019.12.004

Charlier E, Deroyer C, Ciregia F, et al., 2019. Chondrocyte dedifferentiation and osteoarthritis (OA). Biochem Pharmacol, 165:49-65. https://doi.org/10.1016/j.bcp.2019.02.036https://doi.org/10.1016/j.bcp.2019.02.036

Chen G, Han Z, Feng D, et al., 2014. A regulatory signaling loop comprising the PGAM5 phosphatase and CK2 controls receptor-mediated mitophagy. Mol Cell, 54(3):362-377. https://doi.org/10.1016/j.molcel.2014.02.034https://doi.org/10.1016/j.molcel.2014.02.034

Chen M, Chen ZH, Wang YY, et al., 2016. Mitophagy receptor FUNDC1 regulates mitochondrial dynamics and mitophagy. Autophagy, 12(4):689-702. https://doi.org/10.1080/15548627.2016.1151580https://doi.org/10.1080/15548627.2016.1151580

Cheong H, Nair U, Geng JF, 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. https://doi.org/10.1091/mbc.e07-08-0826https://doi.org/10.1091/mbc.e07-08-0826

Collins JA, Wood ST, Nelson KJ, et al., 2016. Oxidative stress promotes peroxiredoxin hyperoxidation and attenuates pro-survival signaling in aging chondrocytes. J Biol Chem, 291(13):6641-6654. https://doi.org/10.1074/jbc.M115.693523https://doi.org/10.1074/jbc.M115.693523

Coryell PR, Diekman BO, Loeser RF, 2021. Mechanisms and therapeutic implications of cellular senescence in osteoarthritis. Nat Rev Rheumatol, 17(1):47-57. https://doi.org/10.1038/s41584-020-00533-7https://doi.org/10.1038/s41584-020-00533-7

Cuervo AM, Bergamini E, Brunk UT, et al., 2005. Autophagy and aging: the importance of maintaining “clean” cells. Autophagy, 1(3):131-140. https://doi.org/10.4161/auto.1.3.2017https://doi.org/10.4161/auto.1.3.2017

Cui AY, Li HZ, Wang DW, et al., 2020. Global, regional prevalence, incidence and risk factors of knee osteoarthritis in population-based studies. EClinicalMedicine, 29:100587. https://doi.org/10.1016/j.eclinm.2020.100587https://doi.org/10.1016/j.eclinm.2020.100587

D'Adamo S, Cetrullo S, Guidotti S, et al., 2020. Spermidine rescues the deregulated autophagic response to oxidative stress of osteoarthritic chondrocytes. Free Radic Biol Med, 153:159-172. https://doi.org/10.1016/j.freeradbiomed.2020.03.029https://doi.org/10.1016/j.freeradbiomed.2020.03.029

Dai SH, Chen T, Wang YH, 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. https://doi.org/10.3390/ijms150814591https://doi.org/10.3390/ijms150814591

D'Amico D, Olmer M, Fouassier AM, et al., 2022. Urolithin A improves mitochondrial health, reduces cartilage degeneration, and alleviates pain in osteoarthritis. Aging Cell, 21(8):e13662. https://doi.org/10.1111/acel.13662https://doi.org/10.1111/acel.13662

Davis JE, Price LL, Lo GH, 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. https://doi.org/10.1007/s00296-017-3802-6https://doi.org/10.1007/s00296-017-3802-6

Dawson TM, Dawson VL, 2017. Mitochondrial mechanisms of neuronal cell death: potential therapeutics. Annu Rev Pharmacol Toxicol, 57:437-454. https://doi.org/10.1146/annurev-pharmtox-010716-105001https://doi.org/10.1146/annurev-pharmtox-010716-105001

Deng R, Wang Y, Bu YH, 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. https://doi.org/10.1186/s10020-022-00490-9https://doi.org/10.1186/s10020-022-00490-9

Duan R, Xie H, Liu ZZ, 2020. The role of autophagy in osteoarthritis. Front Cell Dev Biol, 8:608388. https://doi.org/10.3389/fcell.2020.608388https://doi.org/10.3389/fcell.2020.608388

Duan YM, Fang HB, 2016. RecQL4 regulates autophagy and apoptosis in U2OS cells. Biochem Cell Biol, 94(6):551-559. https://doi.org/10.1139/bcb-2016-0005https://doi.org/10.1139/bcb-2016-0005

Edgar RS, Green EW, Zhao YW, et al., 2012. Peroxiredoxins are conserved markers of circadian rhythms. Nature, 485(7399):459-464. https://doi.org/10.1038/nature11088https://doi.org/10.1038/nature11088

Egan DF, Shackelford DB, Mihaylova MM, et al., 2011. Phosphorylation of ULK1 (hATG1) by AMP-activated protein kinase connects energy sensing to mitophagy. Science, 331(6016):456-461. https://doi.org/10.1126/science.1196371https://doi.org/10.1126/science.1196371

Eyre D, 2002. Articular cartilage and changes in Arthritis: collagen of articular cartilage. Arthritis Res Ther, 4:30. https://doi.org/10.1186/ar380https://doi.org/10.1186/ar380

Feng XF, Pan JY, Li JY, et al., 2020. Metformin attenuates cartilage degeneration in an experimental osteoarthritis model by regulating AMPK/mTOR. Aging (Albany NY), 12(2):1087-1103. https://doi.org/10.18632/aging.102635https://doi.org/10.18632/aging.102635

Fernández-Moreno M, Rego-Pérez I, Blanco FJ, 2022. Is osteoarthritis a mitochondrial disease? What is the evidence? Curr Opin Rheumatol, 34(1):46-53. https://doi.org/10.1097/bor.0000000000000855https://doi.org/10.1097/bor.0000000000000855

Fivenson EM, Lautrup S, Sun N, et al., 2017. Mitophagy in neurodegeneration and aging. Neurochem Int, 109:202-209. https://doi.org/10.1016/j.neuint.2017.02.007https://doi.org/10.1016/j.neuint.2017.02.007

Friedman JR, Nunnari J, 2014. Mitochondrial form and function. Nature, 505(7483):335-343. https://doi.org/10.1038/nature12985https://doi.org/10.1038/nature12985

Furuya N, Kakuta S, Sumiyoshi K, et al., 2018. NDP52 interacts with mitochondrial RNA poly(A) polymerase to promote mitophagy. EMBO Rep, 19(12):e46363. https://doi.org/10.15252/embr.201846363https://doi.org/10.15252/embr.201846363

Glick D, Barth S, Macleod KF, 2010. Autophagy: cellular and molecular mechanisms. J Pathol, 221(1):3-12. https://doi.org/10.1002/path.2697https://doi.org/10.1002/path.2697

Glyn-Jones S, Palmer AJR, Agricola R, et al., 2015. Osteoarthritis. Lancet, 386(9991):376-387. https://doi.org/10.1016/s0140-6736(14)60802-3https://doi.org/10.1016/s0140-6736(14)60802-3

Hanna RA, Quinsay MN, Orogo AM, 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. https://doi.org/10.1074/jbc.M111.322933https://doi.org/10.1074/jbc.M111.322933

Hardie DG, 2014. AMP-activated protein kinase: maintaining energy homeostasis at the cellular and whole-body levels. Annu Rev Nutr, 34:31-55. https://doi.org/10.1146/annurev-nutr-071812-161148https://doi.org/10.1146/annurev-nutr-071812-161148

He J, He J, 2023. Baicalin mitigated IL-1β-induced osteoarthritis chondrocytes damage through activating mitophagy. Chem Biol Drug Des, 101(6):1322-1334. https://doi.org/10.1111/cbdd.14215https://doi.org/10.1111/cbdd.14215

He YZ, Wu ZP, Xu LH, et al., 2020. The role of SIRT3-mediated mitochondrial homeostasis in osteoarthritis. Cell Mol Life Sci, 77(19):3729-3743. https://doi.org/10.1007/s00018-020-03497-9https://doi.org/10.1007/s00018-020-03497-9

Herzig S, Shaw RJ, 2018. AMPK: guardian of metabolism and mitochondrial homeostasis. Nat Rev Mol Cell Biol, 19(2):121-135. https://doi.org/10.1038/nrm.2017.95https://doi.org/10.1038/nrm.2017.95

Higuchi-Sanabria R, Frankino PA, Paul JW III, et al., 2018. A futile battle? Protein quality control and the stress of aging. Dev Cell, 44(2):139-163. https://doi.org/10.1016/j.devcel.2017.12.020https://doi.org/10.1016/j.devcel.2017.12.020

Hu SL, Zhang CW, Ni LB, et al., 2020. Stabilization of HIF-1α alleviates osteoarthritis via enhancing mitophagy. Cell Death Dis, 11(6):481. https://doi.org/10.1038/s41419-020-2680-0https://doi.org/10.1038/s41419-020-2680-0

Huang LW, Huang TC, Hu YC, et al., 2020. Zinc protects chondrocytes from monosodium iodoacetate-induced damage by enhancing ATP and mitophagy. Biochem Biophys Res Commun, 521(1):50-56. https://doi.org/10.1016/j.bbrc.2019.10.066https://doi.org/10.1016/j.bbrc.2019.10.066

Hunter W, 1995. Of the structure and disease of articulating cartilages. Clin Orthop Relat Res, (317):3-6.

Ibrahim BA, Alenazi FSH, Briski KP, 2015. Energy status determines hindbrain signal transduction pathway transcriptional reactivity to AMPK in the estradiol-treated ovariectomized female rat. Neuroscience, 284:888-899. https://doi.org/10.1016/j.neuroscience.2014.10.068https://doi.org/10.1016/j.neuroscience.2014.10.068

Imhof H, Sulzbacher I, Grampp S, et al., 2000. Subchondral bone and cartilage disease: a rediscovered functional unit. Invest Radiol, 35(10):581-588. https://doi.org/10.1097/00004424-200010000-00004https://doi.org/10.1097/00004424-200010000-00004

Jiang N, Xing BZ, Peng R, et al., 2022. Inhibition of Cpt1a alleviates oxidative stress-induced chondrocyte senescence via regulating mitochondrial dysfunction and activating mitophagy. Mech Ageing Dev, 205:111688. https://doi.org/10.1016/j.mad.2022.111688https://doi.org/10.1016/j.mad.2022.111688

Jin ZZ, Chang BH, Wei YL, et al., 2022. Curcumin exerts chondroprotective effects against osteoarthritis by promoting AMPK/PINK1/Parkin-mediated mitophagy. Biomed Pharmacother, 151:113092. https://doi.org/10.1016/j.biopha.2022.113092https://doi.org/10.1016/j.biopha.2022.113092

Jones DP, 2015. Redox theory of aging. Redox Biol, 5:71-79. https://doi.org/10.1016/j.redox.2015.03.004https://doi.org/10.1016/j.redox.2015.03.004

Kawamata T, Kamada Y, Kabeya Y, et al., 2008. Organization of the pre-autophagosomal structure responsible for autophagosome formation. Mol Biol Cell, 19(5):2039-2050. https://doi.org/10.1091/mbc.e07-10-1048https://doi.org/10.1091/mbc.e07-10-1048

Kerr JS, Adriaanse BA, Greig NH, et al., 2017. Mitophagy and Alzheimer’s disease: cellular and molecular mechanisms. Trends Neurosci, 40(3):151-166. https://doi.org/10.1016/j.tins.2017.01.002https://doi.org/10.1016/j.tins.2017.01.002

Kiaer T, Grønlund J, Sørensen KH, 1988. Subchondral pO2, pCO2, pressure, pH, and lactate in human osteoarthritis of the hip. Clin Orthop Relat Res, (229):149-155.

Kiani C, Chen LW, Wu YJ, et al., 2002. Structure and function of aggrecan. Cell Res, 12(1):19-32. https://doi.org/10.1038/sj.cr.7290106https://doi.org/10.1038/sj.cr.7290106

Kim C, Nevitt M, Guermazi A, 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. https://doi.org/10.1002/art.40537https://doi.org/10.1002/art.40537

Kim D, Song J, Jin EJ, 2021. BNIP3-dependent mitophagy via PGC1α promotes cartilage degradation. Cells, 10(7):1839. https://doi.org/10.3390/cells10071839https://doi.org/10.3390/cells10071839

Kim HA, Suh DI, Song YW, 2001. Relationship between chondrocyte apoptosis and matrix depletion in human articular cartilage. J Rheumatol, 28(9):2038-2045.

Kimura S, Noda T, Yoshimori T, 2008. Dynein-dependent movement of autophagosomes mediates efficient encounters with lysosomes. Cell Struct Funct, 33(1):109-122. https://doi.org/10.1247/csf.08005https://doi.org/10.1247/csf.08005

Kop'eva TN, Bel'skaia OB, Astapenko MG, et al., 1986. Morphology of articular cartilage in osteoarthrosis. Arkh Patol, 48(12):40-46 (in Russian).

Koyano F, Okatsu K, Kosako H, et al., 2014. Ubiquitin is phosphorylated by PINK1 to activate parkin. Nature, 510(7503):162-166. https://doi.org/10.1038/nature13392https://doi.org/10.1038/nature13392

Lazarou M, Sliter DA, Kane LA, et al., 2015. The ubiquitin kinase PINK1 recruits autophagy receptors to induce mitophagy. Nature, 524(7565):309-314. https://doi.org/10.1038/nature14893https://doi.org/10.1038/nature14893

Lei QY, Tan J, Yi SQ, 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. https://doi.org/10.1186/s11658-018-0081-5https://doi.org/10.1186/s11658-018-0081-5

Liu D, Cai ZJ, Yang YT, et al., 2022. Mitochondrial quality control in cartilage damage and osteoarthritis: new insights and potential therapeutic targets. Osteoarthritis Cartilage, 30(3):395-405. https://doi.org/10.1016/j.joca.2021.10.009https://doi.org/10.1016/j.joca.2021.10.009

Liu L, Feng D, Chen G, et al., 2012. Mitochondrial outer-membrane protein FUNDC1 mediates hypoxia-induced mitophagy in mammalian cells. Nat Cell Biol, 14(2):177-185. https://doi.org/10.1038/ncb2422https://doi.org/10.1038/ncb2422

Liu L, Zhang WY, Liu TH, et al., 2023. The physiological metabolite α-ketoglutarate ameliorates osteoarthritis by regulating mitophagy and oxidative stress. Redox Biol, 62:102663. https://doi.org/10.1016/j.redox.2023.102663https://doi.org/10.1016/j.redox.2023.102663

Lombard DB, Alt FW, Cheng HL, et al., 2007. Mammalian Sir2 homolog SIRT3 regulates global mitochondrial lysine acetylation. Mol Cell Biol, 27(24):8807-8814. https://doi.org/10.1128/mcb.01636-07https://doi.org/10.1128/mcb.01636-07

Lu JR, Peng Y, Zou JP, et al., 2021. Hypoxia inducible factor-1α is a regulator of autophagy in osteoarthritic chondrocytes. Cartilage, 13(2_suppl):1030s-1040s. https://doi.org/10.1177/19476035211035434https://doi.org/10.1177/19476035211035434

Ma ZT, Wang DL, Weng J, 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. https://doi.org/10.1186/s13018-020-01791-7https://doi.org/10.1186/s13018-020-01791-7

Maimaitijuma T, Yu JH, Ren YL, et al., 2020. PHF23 negatively regulates the autophagy of chondrocytes in osteoarthritis. Life Sci, 253:117750. https://doi.org/10.1016/j.lfs.2020.117750https://doi.org/10.1016/j.lfs.2020.117750

Matsuhashi T, Sato T, Kanno SI, et al., 2017. Mitochonic acid 5 (MA-5) facilitates ATP synthase oligomerization and cell survival in various mitochondrial diseases. eBioMedicine, 20:27-38. https://doi.org/10.1016/j.ebiom.2017.05.016https://doi.org/10.1016/j.ebiom.2017.05.016

Mei RH, Lou P, You GC, et al., 2021. 17β-Estradiol induces mitophagy upregulation to protect chondrocytes via the SIRT1-mediated AMPK/mTOR signaling pathway. Front Endocrinol (Lausanne), 11:615250. https://doi.org/10.3389/fendo.2020.615250https://doi.org/10.3389/fendo.2020.615250

Miwa S, Kashyap S, Chini E, et al., 2022. Mitochondrial dysfunction in cell senescence and aging. J Clin Invest, 132(13):e158447. https://doi.org/10.1172/jci158447https://doi.org/10.1172/jci158447

Najafipour H, Ferrell WR, 1995. Comparison of synovial PO2 and sympathetic vasoconstrictor responses in normal and acutely inflamed rabbit knee joints. Exp Physiol, 80(2):209-220. https://doi.org/10.1113/expphysiol.1995.sp003841https://doi.org/10.1113/expphysiol.1995.sp003841

Nguyen TN, Padman BS, Lazarou M, 2016. Deciphering the molecular signals of PINK1/Parkin mitophagy. Trends Cell Biol, 26(10):733-744. https://doi.org/10.1016/j.tcb.2016.05.008https://doi.org/10.1016/j.tcb.2016.05.008

Novak I, Kirkin V, McEwan DG, et al., 2010. Nix is a selective autophagy receptor for mitochondrial clearance. EMBO Rep, 11(1):45-51. https://doi.org/10.1038/embor.2009.256https://doi.org/10.1038/embor.2009.256

Paulsson M, Heinegård D, 1979. Matrix proteins bound to associatively prepared proteoglycans from bovine cartilage. Biochem J, 183(3):539-545. https://doi.org/10.1042/bj1830539https://doi.org/10.1042/bj1830539

Pedro JMBS, Kroemer G, Galluzzi L, 2017. Autophagy and mitophagy in cardiovascular disease. Circ Res, 120(11):1812-1824. https://doi.org/10.1161/circresaha.117.311082https://doi.org/10.1161/circresaha.117.311082

Petursson F, Husa M, June R, 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. https://doi.org/10.1186/ar4254https://doi.org/10.1186/ar4254

Pfander D, Gelse K, 2007. Hypoxia and osteoarthritis: how chondrocytes survive hypoxic environments. Curr Opin Rheumatol, 19(5):457-462. https://doi.org/10.1097/BOR.0b013e3282ba5693https://doi.org/10.1097/BOR.0b013e3282ba5693

Qin N, Wei LW, Li WY, 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. https://doi.org/10.1016/j.jphs.2017.06.002https://doi.org/10.1016/j.jphs.2017.06.002

Reed KN, Wilson G, Pearsall A, et al., 2014. The role of mitochondrial reactive oxygen species in cartilage matrix destruction. Mol Cell Biochem, 397(1-2):195-201. https://doi.org/10.1007/s11010-014-2187-zhttps://doi.org/10.1007/s11010-014-2187-z

Russell EM, Miller RH, Umberger BR, et al., 2013. Lateral wedges alter mediolateral load distributions at the knee joint in obese individuals. J Orthop Res, 31(5):665-671. https://doi.org/10.1002/jor.22248https://doi.org/10.1002/jor.22248

Salucci S, Falcieri E, Battistelli M, 2022. Chondrocyte death involvement in osteoarthritis. Cell Tissue Res, 389(2):159-170. https://doi.org/10.1007/s00441-022-03639-4https://doi.org/10.1007/s00441-022-03639-4

Sarraf SA, Raman M, Guarani-Pereira V, et al., 2013. Landscape of the PARKIN-dependent ubiquitylome in response to mitochondrial depolarization. Nature, 496(7445):372-376. https://doi.org/10.1038/nature12043https://doi.org/10.1038/nature12043

Scherz-Shouval R, Shvets E, Fass E, et al., 2007. Reactive oxygen species are essential for autophagy and specifically regulate the activity of Atg4. EMBO J, 26(7):1749-1760. https://doi.org/10.1038/sj.emboj.7601623https://doi.org/10.1038/sj.emboj.7601623

Schulz RM, Bader A, 2007. Cartilage tissue engineering and bioreactor systems for the cultivation and stimulation of chondrocytes. Eur Biophys J, 36(4-5):539-568. https://doi.org/10.1007/s00249-007-0139-1https://doi.org/10.1007/s00249-007-0139-1

Shang J, Lin N, Peng R, et al., 2023. Inhibition of Klf10 attenuates oxidative stress-induced senescence of chondrocytes via modulating mitophagy. Molecules, 28(3):924. https://doi.org/10.3390/molecules28030924https://doi.org/10.3390/molecules28030924

Shin HJ, Park H, Shin N, et al., 2019. Pink1-mediated chondrocytic mitophagy contributes to cartilage degeneration in osteoarthritis. J Clin Med, 8(11):1849. https://doi.org/10.3390/jcm8111849https://doi.org/10.3390/jcm8111849

Sowter HM, Ratcliffe PJ, Watson P, 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.

Stolz A, Ernst A, Dikic I, 2014. Cargo recognition and trafficking in selective autophagy. Nat Cell Biol, 16(6):495-501. https://doi.org/10.1038/ncb2979https://doi.org/10.1038/ncb2979

Sun K, Jing XZ, Guo JC, et al., 2021. Mitophagy in degenerative joint diseases. Autophagy, 17(9):2082-2092. https://doi.org/10.1080/15548627.2020.1822097https://doi.org/10.1080/15548627.2020.1822097

Suzuki K, Kirisako T, Kamada Y, 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. https://doi.org/10.1093/emboj/20.21.5971https://doi.org/10.1093/emboj/20.21.5971

Suzuki K, Akioka M, Kondo-Kakuta C, et al., 2013. Fine mapping of autophagy-related proteins during autophagosome formation in Saccharomyces cerevisiae. J Cell Sci, 126(Pt 11):2534-2544. https://doi.org/10.1242/jcs.122960https://doi.org/10.1242/jcs.122960

Tahrir FG, Langford D, Amini S, 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. https://doi.org/10.1002/jcp.27597https://doi.org/10.1002/jcp.27597

Tamrakar P, Ibrahim BA, Gujar AD, 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. https://doi.org/10.1002/jnr.23481https://doi.org/10.1002/jnr.23481

Tang Q, Zheng G, Feng ZH, 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. https://doi.org/10.1038/cddis.2017.453https://doi.org/10.1038/cddis.2017.453

Tian WL, Li W, Chen YQ, et al., 2015. Phosphorylation of ULK1 by AMPK regulates translocation of ULK1 to mitochondria and mitophagy. FEBS Lett, 589(15):1847-1854. https://doi.org/10.1016/j.febslet.2015.05.020https://doi.org/10.1016/j.febslet.2015.05.020

Vadalà G, di Giacomo G, Ambrosio L, et al., 2020. Irisin recovers osteoarthritic chondrocytes in vitro. Cells, 9(6):1478. https://doi.org/10.3390/cells9061478https://doi.org/10.3390/cells9061478

Vina ER, Kwoh CK, 2018. Epidemiology of osteoarthritis: literature update. Curr Opin Rheumatol, 30(2):160-167. https://doi.org/10.1097/BOR.0000000000000479https://doi.org/10.1097/BOR.0000000000000479

Wang CZ, Yang Y, Zhang YQ, 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. https://doi.org/10.5582/bst.2018.01263https://doi.org/10.5582/bst.2018.01263

Wang FS, Kuo CW, Ko JY, et al., 2020. Irisin mitigates oxidative stress, chondrocyte dysfunction and osteoarthritis development through regulating mitochondrial integrity and autophagy. Antioxidants (Basel), 9(9):810. https://doi.org/10.3390/antiox9090810https://doi.org/10.3390/antiox9090810

Wang JL, Wang K, Huang CA, et al., 2018. SIRT3 activation by dihydromyricetin suppresses chondrocytes degeneration via maintaining mitochondrial homeostasis. Int J Biol Sci, 14(13):1873-1882. https://doi.org/10.7150/ijbs.27746https://doi.org/10.7150/ijbs.27746

Wang S, Deng ZT, Ma YC, et al., 2020. The role of autophagy and mitophagy in bone metabolic disorders. Int J Biol Sci, 16(14):2675-2691. https://doi.org/10.7150/ijbs.46627https://doi.org/10.7150/ijbs.46627

Wang WF, Liu SY, Qi ZF, 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. https://doi.org/10.26355/eurrev_202008_22622https://doi.org/10.26355/eurrev_202008_22622

Wang YQ, Serricchio M, Jauregui M, et al., 2015. Deubiquitinating enzymes regulate PARK2-mediated mitophagy. Autophagy, 11(4):595-606. https://doi.org/10.1080/15548627.2015.1034408https://doi.org/10.1080/15548627.2015.1034408

Williams JA, Zhao K, Jin SK, et al., 2017. New methods for monitoring mitochondrial biogenesis and mitophagy in vitro and in vivo. Exp Biol Med (Maywood), 242(8):781-787. https://doi.org/10.1177/1535370216688802https://doi.org/10.1177/1535370216688802

Wu LH, Liu HQ, Li LF, et al., 2014. Mitochondrial pathology in osteoarthritic chondrocytes. Curr Drug Targets, 15(7):710-719. https://doi.org/10.2174/1389450115666140417120305https://doi.org/10.2174/1389450115666140417120305

Wu WX, Tian WL, Hu Z, et al., 2014. ULK1 translocates to mitochondria and phosphorylates FUNDC1 to regulate mitophagy. EMBO Rep, 15(5):566-575. https://doi.org/10.1002/embr.201438501https://doi.org/10.1002/embr.201438501

Xian HX, Watari K, Sanchez-Lopez E, 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. https://doi.org/10.1016/j.immuni.2022.06.007https://doi.org/10.1016/j.immuni.2022.06.007

Xin RB, Xu YY, Long DB, 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. https://doi.org/10.3389/fphar.2022.911716https://doi.org/10.3389/fphar.2022.911716

Xu L, Wu Z, He Y, et al., 2020. MFN2 contributes to metabolic disorders and inflammation in the aging of rat chondrocytes and osteoarthritis. Osteoarthritis Cartilage, 28(8):1079-1091. https://doi.org/10.1016/j.joca.2019.11.011https://doi.org/10.1016/j.joca.2019.11.011

Xu WN, Yang RZ, Zheng HL, 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. https://doi.org/10.1016/j.ijbiomac.2019.06.163https://doi.org/10.1016/j.ijbiomac.2019.06.163

Yamamoto H, Fujioka Y, Suzuki SW, et al., 2016. The intrinsically disordered protein Atg13 mediates supramolecular assembly of autophagy initiation complexes. Dev Cell, 38(1):86-99. https://doi.org/10.1016/j.devcel.2016.06.015https://doi.org/10.1016/j.devcel.2016.06.015

Yu WJ, Gao BL, Li N, 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. https://doi.org/10.1016/j.bbadis.2016.10.021https://doi.org/10.1016/j.bbadis.2016.10.021

Yu XB, Chen GY, Zhou L, et al., 2022. Chondroprotective effects of Gubitong recipe via inhibiting excessive mitophagy of chondrocytes. Evid Based Complement Alternat Med, 2022:8922021. https://doi.org/10.1155/2022/8922021https://doi.org/10.1155/2022/8922021

Zhang XJ, Chen S, Song L, 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. https://doi.org/10.4161/auto.27710https://doi.org/10.4161/auto.27710

Zhang YJ, Liu Y, Hou MZ, et al., 2023. Reprogramming of mitochondrial respiratory chain complex by targeting SIRT3-COX4I2 axis attenuates osteoarthritis progression. Adv Sci (Weinh), 10(10):2206144. https://doi.org/10.1002/advs.202206144https://doi.org/10.1002/advs.202206144

Views

Downloads

CSCD

Tools

Publicity Resources

Micropeptides: origins, identification, and potential role in metabolism-related diseases

CircRNA.0007127 triggers apoptosis through the miR-513a-5p/CASP8 axis in K-562 cells

Toxoplasma gondii infection induces cell apoptosis via multiple pathways revealed by transcriptome analysis

Transition of autophagy and apoptosis in fibroblasts depends on dominant expression of HIF-1α or p53

Blocking the JAK2/STAT3 and ERK pathways suppresses the proliferation of gastrointestinal cancers by inducing apoptosis

Related Author

No data

Related Institution

School of Basic Medicine Sciences, Weifang Medical University

School of Medicine, South China University of Technology

Department of Blood Transfusion, the Second Affiliation Hospital of South China University of Technology

Guangdong Engineering Research Center of Precise Transfusion

Department of Blood Transfusion, Shenzhen Longhua Central Hospital

Address：Journal of Zhejiang University-SCIENCE, 38 Zheda Road, Hangzhou, China Postal code：310027
Tel：+86-571-87952783 Email：cjzhang@zju.edu.cn
Technical support is provided by Beijing Founder electronics co., LTD 京ICP备09064830号-19 京公网安备11010802024621
It is recommended to read the content of this site in Chrome&IE9+. Please switch to extreme mode in browser 360.
Cookies We use cookies to help provide and enhance our service and tailor content. By continuing, you agree to the use of cookies.

⁰