粒体自噬
线粒体生物发生
线粒体
骨关节炎
活性氧
医学
氧化应激
线粒体DNA
氧化磷酸化
机制(生物学)
生物信息学
生物
细胞生物学
神经科学
自噬
内科学
病理
遗传学
生物化学
基因
细胞凋亡
哲学
替代医学
认识论
作者
Chiyuen Cheung,Shaoqin Tu,Yi Feng,Chuiming Wan,Hong Ai,Zheng Chen
标识
DOI:10.1016/j.archger.2024.105522
摘要
Osteoarthritis (OA) is a prevalent chronic joint disease characterized by articular cartilage degeneration, pain, and disability. Emerging evidence indicates that mitochondrial quality control dysfunction contributes to OA pathogenesis. Mitochondria are essential organelles to generate cellular energy via oxidative phosphorylation and regulate vital processes. Impaired mitochondria can negatively impact cellular metabolism and result in the generation of harmful reactive oxygen species (ROS). Dysfunction in mitochondrial quality control mechanisms has been increasingly linked to OA onset and progression. This review summarizes current knowledge on the role of mitochondrial quality control disruption in OA, highlighting disturbed mitochondrial dynamics, impaired mitochondrial biogenesis, antioxidant defenses and mitophagy. The review also discusses potential therapeutic strategies targeting mitochondrial Quality Control in OA, offering future perspectives on advancing OA therapeutic strategies.
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