线粒体
自噬
骨关节炎
生物
发病机制
氧化应激
疾病
滑膜关节
生物信息学
细胞代谢
人口
医学
细胞生物学
新陈代谢
关节软骨
免疫学
病理
内分泌学
遗传学
细胞凋亡
替代医学
环境卫生
作者
Zhanhai Qi,Jiaping Zhu,Wusheng Cai,Chunbiao Lou,Zongyu Li
标识
DOI:10.1007/s11010-023-04818-9
摘要
Osteoarthritis (OA), a prevalent degenerative joint disease, affects a substantial global population. Despite the elusive etiology of OA, recent investigations have implicated mitochondrial dysfunction as a significant factor in disease pathogenesis. Mitochondria, pivotal cellular organelles accountable for energy production, exert essential roles in cellular metabolism. Hence, mitochondrial dysfunction can exert broad-ranging effects on various cellular processes implicated in OA development. This comprehensive review aims to provide an overview of the metabolic alterations occurring in OA and elucidate the diverse mechanisms through which mitochondrial dysfunction can contribute to OA pathogenesis. These mechanisms encompass heightened oxidative stress and inflammation, perturbed chondrocyte metabolism, and compromised autophagy. Furthermore, this review will explore potential interventions targeting mitochondrial metabolism as means to impede or decelerate the progression of OA. In summary, this review offers a comprehensive understanding of the involvement of mitochondrial metabolism in OA and underscores prospective intervention strategies.
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