粒体自噬
骨关节炎
自噬
变性(医学)
线粒体
医学
软骨
滑膜关节
平衡
生物
生物信息学
细胞生物学
关节软骨
病理
内科学
解剖
细胞凋亡
遗传学
替代医学
作者
Hong Cao,Xuchang Zhou,Bowen Xu,Hongmin Hu,Jianming Guo,Miao Wang,Nan Li,Jun Zou
出处
期刊:Journal of Zhejiang University-science B
[Springer Nature]
日期:2024-03-01
卷期号:25 (3): 197-211
被引量:2
标识
DOI:10.1631/jzus.b2300402
摘要
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.
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