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2022, Vol. 26 ›› Issue (9): 1452-1458Osteoarthritis and mitochondrial abnormalitiesJin Tao1, Liu Lin2, Zhu Xiaoyan1, Shi Yucong1, Niu Jianxiong1, Zhang Tongtong1, Wu Shujin3, Yang Qingshan2
Abstract: BACKGROUND: Osteoarthritis is a chronic and progressive joint degenerative disease associated with multiple factors, and the role of mitochondria in osteoarthritis should not be ignored. OBJECTIVE: To review the current relevant literature, summarize the relationship between mitochondria and osteoarthritis, understand the mechanism of mitochondrial damage in the pathogenesis of osteoarthritis, and provide theoretical reference for the treatment of osteoarthritis through mitochondrial pathway. METHODS: The key words were “mitochondria; mitochondrial; osteoarthritis; ostarthritis; ostearthritis”. The retrieval formula was “(mitochondria) OR (mitochondrial) AND (osteoarthritis) OR (ostarthritis) OR (ostearthritis)” on PubMed database. 455 articles published from 2000 to 2021 were primarily retrieved. According to the inclusion and exclusion criteria, 61 articles were finally included for review. RESULTS AND CONCLUSION: (1) Mitochondria play a key role in osteoarthritis. Abnormal mitochondrial REDOX can inhibit matrix synthesis, activate matrix metalloproteinase to degrade matrix components, induce cytokine production and chondrocyte apoptosis, and promote cartilage degeneration. Lack of biogenesis leads to accelerated prechondrocyte catabolism. When the kinetics is abnormal, damaged mitochondria accumulate, which leads to the inability of mitochondria to produce enough biological energy, regulate calcium and maintain a REDOX state, thereby accelerating the development of osteoarthritis. When mitosis is damaged, the dysfunctional mitochondria cannot be cleared in time, leading to the disorder of mitochondrial dynamic balance. Genetic abnormalities lead to increased mitochondrial respiration and glycolysis, increased production of free radicals and pro-inflammatory cytokines, and increased apoptosis resulting in chondrocyte dysfunction. However, abnormal calcium regulation will lead to excessive production of reactive oxygen species, mitochondrial depolarization and decreased mitochondrial membrane potential, which will lead to chondrocyte apoptosis. (2) In the treatment of osteoarthritis, drugs targeting endogenous AMPK, SIRT and Parkin, as well as exogenous antioxidants that can inhibit mitochondrial apoptosis and enhance mitochondrial dynamics are expected to become potential drugs for the early treatment of osteoarthritis. Key words:osteoarthritis, mitochondria">, reactive oxygen species">, biogenesis">, mitochondrial dynamics">, mitochondrial DNA">, calcium">, review |