Research progress of optic atrophy 1-mediated mitochondrial dynamics in skeletal system diseases_Chinese Journal of Reparative and Reconstructive Surgery

Authors：

SUN Kaibo , WU Yuangang , ZENG Yi , LI Mingyang , WU Limin ,  SHEN Bin

Department of Orthopedics, Orthopedic Research Institute, West China Hospital, Sichuan University, Chengdu Sichuan, 610041, P. R. China;

Corresponding author：

SHEN Bin, Email: shenbin_1971@163.com

Keywords：

Mitochondrial quality control; mitochondrial dynamics; optic atrophy 1; disorder of skeletal system

DOI：

10.7507/1002-1892.202302056

Video：

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Abstract Full text Figures/Tables Video References Cited by

Objective To review the research progress of mitochondrial dynamics mediated by optic atrophy 1 (OPA1) in skeletal system diseases. Methods The literatures about OPA1-mediated mitochondrial dynamics in recent years were reviewed, and the bioactive ingredients and drugs for the treatment of skeletal system diseases were summarized, which provided a new idea for the treatment of osteoarthritis. Results OPA1 is a key factor involved in mitochondrial dynamics and energetics and in maintaining the stability of the mitochondrial genome. Accumulating evidence indicates that OPA1-mediated mitochondrial dynamics plays an important role in the regulation of skeletal system diseases such as osteoarthritis, osteoporosis, and osteosarcoma. Conclusion OPA1-mediated mitochondrial dynamics provides an important theoretical basis for the prevention and treatment of skeletal system diseases.

Citation： SUN Kaibo, WU Yuangang, ZENG Yi, LI Mingyang, WU Limin, SHEN Bin. Research progress of optic atrophy 1-mediated mitochondrial dynamics in skeletal system diseases. Chinese Journal of Reparative and Reconstructive Surgery, 2023, 37(6): 758-763. doi: 10.7507/1002-1892.202302056 Copy

1.	Nunnari J, Suomalainen A. Mitochondria: in sickness and in health. Cell, 2012, 148(6): 1145-1159.
2.	Liu D, Cai ZJ, Yang YT, et al. Mitochondrial quality control in cartilage damage and osteoarthritis: new insights and potential therapeutic targets. Osteoarthritis Cartilage, 2022, 30(3): 395-405.
3.	Chen LY, Wang Y, Terkeltaub R, et al. Activation of AMPK-SIRT3 signaling is chondroprotective by preserving mitochondrial DNA integrity and function. Osteoarthritis Cartilage, 2018, 26(11): 1539-1550.
4.	Chen Y, Wu YY, Si HB, et al. Mechanistic insights into AMPK-SIRT3 positive feedback loop-mediated chondrocyte mitochondrial quality control in osteoarthritis pathogenesis. Pharmacol Res, 2021, 166: 105497. doi: 10.1016/j.phrs.2021.105497.
5.	Vega RB, Horton JL, Kelly DP. Maintaining ancient organelles: mitochondrial biogenesis and maturation. Circ Res, 2015, 116(11): 1820-1834.
6.	Sun K, Jing X, Guo J, et al. Mitophagy in degenerative joint diseases. Autophagy, 2021, 17(9): 2082-2092.
7.	Archer SL. Mitochondrial dynamics-mitochondrial fission and fusion in human diseases. N Engl J Med, 2013, 369(23): 2236-2251.
8.	Eisner V, Picard M, Hajnóczky G. Mitochondrial dynamics in adaptive and maladaptive cellular stress responses. Nat Cell Biol, 2018, 20(7): 755-765.
9.	He Y, Wu Z, Xu L, et al. The role of SIRT3-mediated mitochon-drial homeostasis in osteoarthritis. Cell Mol Life Sci, 2020, 77(19): 3729-3743.
10.	Chen H, Chomyn A, Chan DC. Disruption of fusion results in mitochondrial heterogeneity and dysfunction. J Biol Chem, 2005, 280(28): 26185-26192.
11.	Olichon A, Baricault L, Gas N, et al. Loss of OPA1 perturbates the mitochondrial inner membrane structure and integrity, leading to cytochrome c release and apoptosis. J Biol Chem, 2003, 278(10): 7743-7746.
12.	Alexander C, Votruba M, Pesch UE, et al. OPA1, encoding a dynamin-related GTPase, is mutated in autosomal dominant optic atrophy linked to chromosome 3q28. Nat Genet, 2000, 26(2): 211-215.
13.	Pesch UE, Leo-Kottler B, Mayer S, et al. OPA1 mutations in patients with autosomal dominant optic atrophy and evidence for semi-dominant inheritance. Hum Mol Genet, 2001, 10(13): 1359-1368.
14.	Lenaers G, Reynier P, Elachouri G, et al. OPA1 functions in mitochondria and dysfunctions in optic nerve. Int J Biochem Cell Biol, 2009, 41(10): 1866-1874.
15.	Song Z, Chen H, Fiket M, et al. OPA1 processing controls mitochondrial fusion and is regulated by mRNA splicing, membrane potential, and Yme1L. J Cell Biol, 2007, 178(5): 749-755.
16.	Ehses S, Raschke I, Mancuso G, et al. Regulation of OPA1 processing and mitochondrial fusion by m-AAA protease isoenzymes and OMA1. J Cell Biol, 2009, 187(7): 1023-1036.
17.	MacVicar T, Langer T. OPA1 processing in cell death and disease-the long and short of it. J Cell Sci, 2016, 129(12): 2297-2306.
18.	Ge Y, Shi X, Boopathy S, et al. Two forms of Opa1 cooperate to complete fusion of the mitochondrial inner-membrane. Elife, 2020, 9: e50973. doi: 10.7554/eLife.50973.
19.	Rampelt H, Zerbes RM, van der Laan M, et al. Role of the mitochondrial contact site and cristae organizing system in membrane architecture and dynamics. Biochim Biophys Acta Mol Cell Res, 2017, 1864(4): 737-746.
20.	Frezza C, Cipolat S, Martins de Brito O, et al. OPA1 controls apoptotic cristae remodeling independently from mitochondrial fusion. Cell, 2006, 126(1): 177-189.
21.	Zanna C, Ghelli A, Porcelli AM, et al. OPA1 mutations associated with dominant optic atrophy impair oxidative phosphorylation and mitochondrial fusion. Brain, 2008, 131(Pt 2): 352-367.
22.	Lee H, Smith SB, Yoon Y. The short variant of the mitochondrial dynamin OPA1 maintains mitochondrial energetics and cristae structure. J Biol Chem, 2017, 292(17): 7115-7130.
23.	Kushnareva YE, Gerencser AA, Bossy B, et al. Loss of OPA1 disturbs cellular calcium homeostasis and sensitizes for excitotoxicity. Cell Death Differ, 2013, 20(2): 353-365.
24.	Takahashi K, Ohsawa I, Shirasawa T, et al. Optic atrophy 1 mediates coenzyme Q-responsive regulation of respiratory complex Ⅳ activity in brain mitochondria. Exp Gerontol, 2017, 98: 217-223.
25.	Manini A, Abati E, Comi GP, et al. Mitochondrial DNA homeostasis impairment and dopaminergic dysfunction: A trembling balance. Ageing Res Rev, 2022, 76: 101578. doi: 10.1016/j.arr.2022.101578.
26.	Long J, Huang Y, Tang Z, et al. Mitochondria targeted antioxidant significantly alleviates preeclampsia caused by 11β-HSD2 dysfunction via OPA1 and MtDNA maintenance. Antioxidants (Basel), 2022, 11(8): 1505. doi: 10.3390/antiox11081505.
27.	Elachouri G, Vidoni S, Zanna C, et al. OPA1 links human mitochondrial genome maintenance to mtDNA replication and distribution. Genome Res, 2011, 21(1): 12-20.
28.	Hudson G, Amati-Bonneau P, Blakely EL, et al. Mutation of OPA1 causes dominant optic atrophy with external ophthalmoplegia, ataxia, deafness and multiple mitochondrial DNA deletions: a novel disorder of mtDNA maintenance. Brain, 2008, 131(Pt 2): 329-337.
29.	Chen H, Vermulst M, Wang YE, et al. Mitochondrial fusion is required for mtDNA stability in skeletal muscle and tolerance of mtDNA mutations. Cell, 2010, 141(2): 280-289.
30.	Rahmati M, Nalesso G, Mobasheri A, et al. Aging and osteoarthritis: Central role of the extracellular matrix. Ageing Res Rev, 2017, 40: 20-30.
31.	Xie J, Wang Y, Lu L, et al. Cellular senescence in knee osteoarthritis: molecular mechanisms and therapeutic implications. Ageing Res Rev, 2021, 70: 101413. doi: 10.1016/j.arr.2021.101413.
32.	Coryell PR, Diekman BO, Loeser RF. Mechanisms and therapeutic implications of cellular senescence in osteoarthritis. Nat Rev Rheumatol, 2021, 17(1): 47-57.
33.	Zhang J, Hao X, Chi R, et al. Moderate mechanical stress suppresses the IL-1β-induced chondrocyte apoptosis by regulating mitochondrial dynamics. J Cell Physiol, 2021, 236(11): 7504-7515.
34.	Ansari MY, Khan NM, Ahmad I, et al. Parkin clearance of dysfunctional mitochondria regulates ROS levels and increases survival of human chondrocytes. Osteoarthritis Cartilage, 2018, 26(8): 1087-1097.
35.	Loeser RF, Collins JA, Diekman BO. Ageing and the pathogenesis of osteoarthritis. Nat Rev Rheumatol, 2016, 12(7): 412-420.
36.	Jiang W, Liu H, Wan R, et al. Mechanisms linking mitochondrial mechanotransduction and chondrocyte biology in the pathogenesis of osteoarthritis. Ageing Res Rev, 2021, 67: 101315. doi: 10.1016/j.arr.2021.101315.
37.	Blanco FJ, Valdes AM, Rego-Pérez I. Mitochondrial DNA variation and the pathogenesis of osteoarthritis phenotypes. Nat Rev Rheumatol, 2018, 14(6): 327-340.
38.	Ruiz-Romero C, Calamia V, Mateos J, et al. Mitochondrial dysregulation of osteoarthritic human articular chondrocytes analyzed by proteomics: a decrease in mitochondrial superoxide dismutase points to a redox imbalance. Mol Cell Proteomics, 2009, 8(1): 172-189.
39.	Samant SA, Zhang HJ, Hong Z, et al. SIRT3 deacetylates and activates OPA1 to regulate mitochondrial dynamics during stress. Mol Cell Biol, 2014, 34(5): 807-819.
40.	Sun K, Wu Y, Zeng Y, et al. The role of the sirtuin family in cartilage and osteoarthritis: molecular mechanisms and therapeutic targets. Arthritis Res Ther, 2022, 24(1): 286. doi: 10.1186/s13075-022-02983-8.
41.	Wang J, Wang K, Huang C, et al. SIRT3 activation by dihydromyricetin suppresses chondrocytes degeneration via maintaining mitochondrial homeostasis. Int J Biol Sci, 2018, 14(13): 1873-1882.
42.	Yao X, Zhang J, Jing X, et al. Fibroblast growth factor 18 exerts anti-osteoarthritic effects through PI3K-AKT signaling and mitochondrial fusion and fission. Pharmacol Res, 2019, 139: 314-324.
43.	Kim JM, Lin C, Stavre Z, et al. Osteoblast-osteoclast communication and bone homeostasis. Cells, 2020, 9(9): 2073. doi: 10.3390/cells9092073.
44.	Ensrud KE, Crandall CJ. Osteoporosis. Ann Intern Med, 2017, 167(3): ITC17-ITC32.
45.	Yang YH, Li B, Zheng XF, et al. Oxidative damage to osteoblasts can be alleviated by early autophagy through the endoplasmic reticulum stress pathway-implications for the treatment of osteoporosis. Free Radic Biol Med, 2014, 77: 10-20.
46.	Jia L, Ma T, Lv L, et al. Endoplasmic reticulum stress mediated by ROS participates in cadmium exposure-induced MC3T3-E1 cell apoptosis. Ecotoxicol Environ Saf, 2023, 251: 114517. doi: 10.1016/j.ecoenv.2023.114517.
47.	Cai WJ, Chen Y, Shi LX, et al. AKT-GSK3 β signaling pathway regulates mitochondrial dysfunction-associated opa1 cleavage contributing to osteoblast apoptosis: Preventative effects of hydroxytyrosol. Oxid Med Cell Longev, 2019, 2019: 4101738. doi: 10.1155/2019/4101738.
48.	Bonewald L. Use it or lose it to age: A review of bone and muscle communication. Bone, 2019, 120: 212-218.
49.	Chen M, Wang D, Li M, et al. Nanocatalytic biofunctional MOF coating on titanium implants promotes osteoporotic bone regeneration through cooperative pro-osteoblastogenesis MSC reprogramming. ACS Nano, 2022, 16(9): 15397-15412.
50.	Nagarajan R, Kamruzzaman A, Ness KK, et al. Twenty years of follow-up of survivors of childhood osteosarcoma: a report from the Childhood Cancer Survivor Study. Cancer, 2011, 117(3): 625-634.
51.	Garcia I, Innis-Whitehouse W, Lopez A, et al. Oxidative insults disrupt OPA1-mediated mitochondrial dynamics in cultured mammalian cells. Redox Rep, 2018, 23(1): 160-167.
52.	Huang ST, Huang CC, Sheen JM, et al. Phyllanthus urinaria’s inhibition of human osteosarcoma xenografts growth in mice is associated with modulation of mitochondrial fission/fusion machinery. Am J Chin Med, 2016, 44(7): 1507-1523.
53.	Lai HT, Naumova N, Marchais A, et al. Insight into the interplay between mitochondria-regulated cell death and energetic metabolism in osteosarcoma. Front Cell Dev Biol, 2022, 10: 948097. doi: 10.3389/fcell.2022.948097.
54.	Jones E, Gaytan N, Garcia I, et al. A threshold of transmembrane potential is required for mitochondrial dynamic balance mediated by DRP1 and OMA1. Cell Mol Life Sci, 2017, 74(7): 1347-1363.
55.	Bori Z, Zhao Z, Koltai E, et al. The effects of aging, physical training, and a single bout of exercise on mitochondrial protein expression in human skeletal muscle. Exp Gerontol, 2012, 47(6): 417-424.
56.	Huang DD, Fan SD, Chen XY, et al. Nrf2 deficiency exacerbates frailty and sarcopenia by impairing skeletal muscle mitochondrial biogenesis and dynamics in an age-dependent manner. Exp Gerontol, 2019, 119: 61-73.
57.	Tezze C, Romanello V, Desbats MA, et al. Age-associated loss of OPA1 in muscle impacts muscle mass, metabolic homeostasis, systemic inflammation, and epithelial senescence. Cell Metab, 2017, 25(6): 1374-1389.
58.	Todkar K, Chikhi L, Desjardins V, et al. Selective packaging of mitochondrial proteins into extracellular vesicles prevents the release of mitochondrial DAMPs. Nat Commun, 2021, 12(1): 1971. doi: 10.1038/s41467-021-21984-w.
59.	Wang Y, Li Y, Jiang X, et al. OPA1 supports mitochondrial dynamics and immune evasion to CD8+ T cell in lung adenocarcinoma. PeerJ, 2022, 10: e14543. doi: 10.7717/peerj.14543.
60.	Wang C, Yang Y, Zhang Y, et al. Protective effects of metformin against osteoarthritis through upregulation of SIRT3-mediated PINK1/Parkin-dependent mitophagy in primary chondrocytes. Biosci Trends, 2019, 12(6): 605-612.
61.	Wang FS, Kuo CW, Ko JY, et al. Irisin mitigates oxidative stress, chondrocyte dysfunction and osteoarthritis development through regulating mitochondrial integrity and autophagy. Antioxidants (Basel), 2020, 9(9): 810. doi: 10.3390/antiox9090810.
62.	Wang B, Shao Z, Gu M, et al. Hydrogen sulfide protects against IL-1β-induced inflammation and mitochondrial dysfunction-related apoptosis in chondrocytes and ameliorates osteoarthritis. J Cell Physiol, 2021, 236(6): 4369-4386.
63.	Mao YX, Cai WJ, Sun XY, et al. RAGE-dependent mitochondria pathway: a novel target of silibinin against apoptosis of osteoblastic cells induced by advanced glycation end products. Cell Death Dis, 2018, 9(6): 674. doi: 10.1038/s41419-018-0718-3.

1. Nunnari J, Suomalainen A. Mitochondria: in sickness and in health. Cell, 2012, 148(6): 1145-1159.
2. Liu D, Cai ZJ, Yang YT, et al. Mitochondrial quality control in cartilage damage and osteoarthritis: new insights and potential therapeutic targets. Osteoarthritis Cartilage, 2022, 30(3): 395-405.
3. Chen LY, Wang Y, Terkeltaub R, et al. Activation of AMPK-SIRT3 signaling is chondroprotective by preserving mitochondrial DNA integrity and function. Osteoarthritis Cartilage, 2018, 26(11): 1539-1550.
4. Chen Y, Wu YY, Si HB, et al. Mechanistic insights into AMPK-SIRT3 positive feedback loop-mediated chondrocyte mitochondrial quality control in osteoarthritis pathogenesis. Pharmacol Res, 2021, 166: 105497. doi: 10.1016/j.phrs.2021.105497.
5. Vega RB, Horton JL, Kelly DP. Maintaining ancient organelles: mitochondrial biogenesis and maturation. Circ Res, 2015, 116(11): 1820-1834.
6. Sun K, Jing X, Guo J, et al. Mitophagy in degenerative joint diseases. Autophagy, 2021, 17(9): 2082-2092.
7. Archer SL. Mitochondrial dynamics-mitochondrial fission and fusion in human diseases. N Engl J Med, 2013, 369(23): 2236-2251.
8. Eisner V, Picard M, Hajnóczky G. Mitochondrial dynamics in adaptive and maladaptive cellular stress responses. Nat Cell Biol, 2018, 20(7): 755-765.
9. He Y, Wu Z, Xu L, et al. The role of SIRT3-mediated mitochon-drial homeostasis in osteoarthritis. Cell Mol Life Sci, 2020, 77(19): 3729-3743.
10. Chen H, Chomyn A, Chan DC. Disruption of fusion results in mitochondrial heterogeneity and dysfunction. J Biol Chem, 2005, 280(28): 26185-26192.
11. Olichon A, Baricault L, Gas N, et al. Loss of OPA1 perturbates the mitochondrial inner membrane structure and integrity, leading to cytochrome c release and apoptosis. J Biol Chem, 2003, 278(10): 7743-7746.
12. Alexander C, Votruba M, Pesch UE, et al. OPA1, encoding a dynamin-related GTPase, is mutated in autosomal dominant optic atrophy linked to chromosome 3q28. Nat Genet, 2000, 26(2): 211-215.
13. Pesch UE, Leo-Kottler B, Mayer S, et al. OPA1 mutations in patients with autosomal dominant optic atrophy and evidence for semi-dominant inheritance. Hum Mol Genet, 2001, 10(13): 1359-1368.
14. Lenaers G, Reynier P, Elachouri G, et al. OPA1 functions in mitochondria and dysfunctions in optic nerve. Int J Biochem Cell Biol, 2009, 41(10): 1866-1874.
15. Song Z, Chen H, Fiket M, et al. OPA1 processing controls mitochondrial fusion and is regulated by mRNA splicing, membrane potential, and Yme1L. J Cell Biol, 2007, 178(5): 749-755.
16. Ehses S, Raschke I, Mancuso G, et al. Regulation of OPA1 processing and mitochondrial fusion by m-AAA protease isoenzymes and OMA1. J Cell Biol, 2009, 187(7): 1023-1036.
17. MacVicar T, Langer T. OPA1 processing in cell death and disease-the long and short of it. J Cell Sci, 2016, 129(12): 2297-2306.
18. Ge Y, Shi X, Boopathy S, et al. Two forms of Opa1 cooperate to complete fusion of the mitochondrial inner-membrane. Elife, 2020, 9: e50973. doi: 10.7554/eLife.50973.
19. Rampelt H, Zerbes RM, van der Laan M, et al. Role of the mitochondrial contact site and cristae organizing system in membrane architecture and dynamics. Biochim Biophys Acta Mol Cell Res, 2017, 1864(4): 737-746.
20. Frezza C, Cipolat S, Martins de Brito O, et al. OPA1 controls apoptotic cristae remodeling independently from mitochondrial fusion. Cell, 2006, 126(1): 177-189.
21. Zanna C, Ghelli A, Porcelli AM, et al. OPA1 mutations associated with dominant optic atrophy impair oxidative phosphorylation and mitochondrial fusion. Brain, 2008, 131(Pt 2): 352-367.
22. Lee H, Smith SB, Yoon Y. The short variant of the mitochondrial dynamin OPA1 maintains mitochondrial energetics and cristae structure. J Biol Chem, 2017, 292(17): 7115-7130.
23. Kushnareva YE, Gerencser AA, Bossy B, et al. Loss of OPA1 disturbs cellular calcium homeostasis and sensitizes for excitotoxicity. Cell Death Differ, 2013, 20(2): 353-365.
24. Takahashi K, Ohsawa I, Shirasawa T, et al. Optic atrophy 1 mediates coenzyme Q-responsive regulation of respiratory complex Ⅳ activity in brain mitochondria. Exp Gerontol, 2017, 98: 217-223.
25. Manini A, Abati E, Comi GP, et al. Mitochondrial DNA homeostasis impairment and dopaminergic dysfunction: A trembling balance. Ageing Res Rev, 2022, 76: 101578. doi: 10.1016/j.arr.2022.101578.
26. Long J, Huang Y, Tang Z, et al. Mitochondria targeted antioxidant significantly alleviates preeclampsia caused by 11β-HSD2 dysfunction via OPA1 and MtDNA maintenance. Antioxidants (Basel), 2022, 11(8): 1505. doi: 10.3390/antiox11081505.
27. Elachouri G, Vidoni S, Zanna C, et al. OPA1 links human mitochondrial genome maintenance to mtDNA replication and distribution. Genome Res, 2011, 21(1): 12-20.
28. Hudson G, Amati-Bonneau P, Blakely EL, et al. Mutation of OPA1 causes dominant optic atrophy with external ophthalmoplegia, ataxia, deafness and multiple mitochondrial DNA deletions: a novel disorder of mtDNA maintenance. Brain, 2008, 131(Pt 2): 329-337.
29. Chen H, Vermulst M, Wang YE, et al. Mitochondrial fusion is required for mtDNA stability in skeletal muscle and tolerance of mtDNA mutations. Cell, 2010, 141(2): 280-289.
30. Rahmati M, Nalesso G, Mobasheri A, et al. Aging and osteoarthritis: Central role of the extracellular matrix. Ageing Res Rev, 2017, 40: 20-30.
31. Xie J, Wang Y, Lu L, et al. Cellular senescence in knee osteoarthritis: molecular mechanisms and therapeutic implications. Ageing Res Rev, 2021, 70: 101413. doi: 10.1016/j.arr.2021.101413.
32. Coryell PR, Diekman BO, Loeser RF. Mechanisms and therapeutic implications of cellular senescence in osteoarthritis. Nat Rev Rheumatol, 2021, 17(1): 47-57.
33. Zhang J, Hao X, Chi R, et al. Moderate mechanical stress suppresses the IL-1β-induced chondrocyte apoptosis by regulating mitochondrial dynamics. J Cell Physiol, 2021, 236(11): 7504-7515.
34. Ansari MY, Khan NM, Ahmad I, et al. Parkin clearance of dysfunctional mitochondria regulates ROS levels and increases survival of human chondrocytes. Osteoarthritis Cartilage, 2018, 26(8): 1087-1097.
35. Loeser RF, Collins JA, Diekman BO. Ageing and the pathogenesis of osteoarthritis. Nat Rev Rheumatol, 2016, 12(7): 412-420.
36. Jiang W, Liu H, Wan R, et al. Mechanisms linking mitochondrial mechanotransduction and chondrocyte biology in the pathogenesis of osteoarthritis. Ageing Res Rev, 2021, 67: 101315. doi: 10.1016/j.arr.2021.101315.
37. Blanco FJ, Valdes AM, Rego-Pérez I. Mitochondrial DNA variation and the pathogenesis of osteoarthritis phenotypes. Nat Rev Rheumatol, 2018, 14(6): 327-340.
38. Ruiz-Romero C, Calamia V, Mateos J, et al. Mitochondrial dysregulation of osteoarthritic human articular chondrocytes analyzed by proteomics: a decrease in mitochondrial superoxide dismutase points to a redox imbalance. Mol Cell Proteomics, 2009, 8(1): 172-189.
39. Samant SA, Zhang HJ, Hong Z, et al. SIRT3 deacetylates and activates OPA1 to regulate mitochondrial dynamics during stress. Mol Cell Biol, 2014, 34(5): 807-819.
40. Sun K, Wu Y, Zeng Y, et al. The role of the sirtuin family in cartilage and osteoarthritis: molecular mechanisms and therapeutic targets. Arthritis Res Ther, 2022, 24(1): 286. doi: 10.1186/s13075-022-02983-8.
41. Wang J, Wang K, Huang C, et al. SIRT3 activation by dihydromyricetin suppresses chondrocytes degeneration via maintaining mitochondrial homeostasis. Int J Biol Sci, 2018, 14(13): 1873-1882.
42. Yao X, Zhang J, Jing X, et al. Fibroblast growth factor 18 exerts anti-osteoarthritic effects through PI3K-AKT signaling and mitochondrial fusion and fission. Pharmacol Res, 2019, 139: 314-324.
43. Kim JM, Lin C, Stavre Z, et al. Osteoblast-osteoclast communication and bone homeostasis. Cells, 2020, 9(9): 2073. doi: 10.3390/cells9092073.
44. Ensrud KE, Crandall CJ. Osteoporosis. Ann Intern Med, 2017, 167(3): ITC17-ITC32.
45. Yang YH, Li B, Zheng XF, et al. Oxidative damage to osteoblasts can be alleviated by early autophagy through the endoplasmic reticulum stress pathway-implications for the treatment of osteoporosis. Free Radic Biol Med, 2014, 77: 10-20.
46. Jia L, Ma T, Lv L, et al. Endoplasmic reticulum stress mediated by ROS participates in cadmium exposure-induced MC3T3-E1 cell apoptosis. Ecotoxicol Environ Saf, 2023, 251: 114517. doi: 10.1016/j.ecoenv.2023.114517.
47. Cai WJ, Chen Y, Shi LX, et al. AKT-GSK3 β signaling pathway regulates mitochondrial dysfunction-associated opa1 cleavage contributing to osteoblast apoptosis: Preventative effects of hydroxytyrosol. Oxid Med Cell Longev, 2019, 2019: 4101738. doi: 10.1155/2019/4101738.
48. Bonewald L. Use it or lose it to age: A review of bone and muscle communication. Bone, 2019, 120: 212-218.
49. Chen M, Wang D, Li M, et al. Nanocatalytic biofunctional MOF coating on titanium implants promotes osteoporotic bone regeneration through cooperative pro-osteoblastogenesis MSC reprogramming. ACS Nano, 2022, 16(9): 15397-15412.
50. Nagarajan R, Kamruzzaman A, Ness KK, et al. Twenty years of follow-up of survivors of childhood osteosarcoma: a report from the Childhood Cancer Survivor Study. Cancer, 2011, 117(3): 625-634.
51. Garcia I, Innis-Whitehouse W, Lopez A, et al. Oxidative insults disrupt OPA1-mediated mitochondrial dynamics in cultured mammalian cells. Redox Rep, 2018, 23(1): 160-167.
52. Huang ST, Huang CC, Sheen JM, et al. Phyllanthus urinaria’s inhibition of human osteosarcoma xenografts growth in mice is associated with modulation of mitochondrial fission/fusion machinery. Am J Chin Med, 2016, 44(7): 1507-1523.
53. Lai HT, Naumova N, Marchais A, et al. Insight into the interplay between mitochondria-regulated cell death and energetic metabolism in osteosarcoma. Front Cell Dev Biol, 2022, 10: 948097. doi: 10.3389/fcell.2022.948097.
54. Jones E, Gaytan N, Garcia I, et al. A threshold of transmembrane potential is required for mitochondrial dynamic balance mediated by DRP1 and OMA1. Cell Mol Life Sci, 2017, 74(7): 1347-1363.
55. Bori Z, Zhao Z, Koltai E, et al. The effects of aging, physical training, and a single bout of exercise on mitochondrial protein expression in human skeletal muscle. Exp Gerontol, 2012, 47(6): 417-424.
56. Huang DD, Fan SD, Chen XY, et al. Nrf2 deficiency exacerbates frailty and sarcopenia by impairing skeletal muscle mitochondrial biogenesis and dynamics in an age-dependent manner. Exp Gerontol, 2019, 119: 61-73.
57. Tezze C, Romanello V, Desbats MA, et al. Age-associated loss of OPA1 in muscle impacts muscle mass, metabolic homeostasis, systemic inflammation, and epithelial senescence. Cell Metab, 2017, 25(6): 1374-1389.
58. Todkar K, Chikhi L, Desjardins V, et al. Selective packaging of mitochondrial proteins into extracellular vesicles prevents the release of mitochondrial DAMPs. Nat Commun, 2021, 12(1): 1971. doi: 10.1038/s41467-021-21984-w.
59. Wang Y, Li Y, Jiang X, et al. OPA1 supports mitochondrial dynamics and immune evasion to CD8+ T cell in lung adenocarcinoma. PeerJ, 2022, 10: e14543. doi: 10.7717/peerj.14543.
60. Wang C, Yang Y, Zhang Y, et al. Protective effects of metformin against osteoarthritis through upregulation of SIRT3-mediated PINK1/Parkin-dependent mitophagy in primary chondrocytes. Biosci Trends, 2019, 12(6): 605-612.
61. Wang FS, Kuo CW, Ko JY, et al. Irisin mitigates oxidative stress, chondrocyte dysfunction and osteoarthritis development through regulating mitochondrial integrity and autophagy. Antioxidants (Basel), 2020, 9(9): 810. doi: 10.3390/antiox9090810.
62. Wang B, Shao Z, Gu M, et al. Hydrogen sulfide protects against IL-1β-induced inflammation and mitochondrial dysfunction-related apoptosis in chondrocytes and ameliorates osteoarthritis. J Cell Physiol, 2021, 236(6): 4369-4386.
63. Mao YX, Cai WJ, Sun XY, et al. RAGE-dependent mitochondria pathway: a novel target of silibinin against apoptosis of osteoblastic cells induced by advanced glycation end products. Cell Death Dis, 2018, 9(6): 674. doi: 10.1038/s41419-018-0718-3.

Chinese Journal of Reparative and Reconstructive Surgery

Research progress of optic atrophy 1-mediated mitochondrial dynamics in skeletal system diseases

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