Blanco F J, Fernández-Moreno M
Grupo de Investigación en Reumatología, Instituto de Investigación Biomédica de A Coruña (INIBIC), Agrupación Estratégica CICA-INIBIC, Complexo Hospitalario Universitario de A Coruña (CHUAC), Sergas, Spain; Department of Medicine, Universidade de A Coruña (UDC), A Coruña, Spain.
Department of Medicine, Universidade de A Coruña (UDC), A Coruña, Spain; Centro de Investigación Biomédica en Red, Bioingeniería, Biomateriales y Nanomedicina (CIBER-BBN), Spain.
Osteoarthritis Cartilage. 2020 Aug;28(8):1003-1006. doi: 10.1016/j.joca.2020.03.018. Epub 2020 May 14.
Mitochondrial dysfunction of human articular chondrocytes is considered a hallmark of cartilage degradation and OA pathogenesis. Due to the huge number of cellular processes in which mitochondria is implicated, even in the closed context of cellular respiration, the term mitochondrial function can refer to a variety of features which include fusion and fission, turnover (biogenesis and mitophagy), and plasticity. Mitochondrial biogenesis and mainly mitochondrial fusion and reduced mitophagy, contribute to the metabolic disorder and inflammation that occurs during OA. Reduced MFN2 and increased PARKIN expression represent potential therapeutic targets for the treatment of joint cartilage degradation during the OA process.
人类关节软骨细胞的线粒体功能障碍被认为是软骨降解和骨关节炎发病机制的一个标志。由于线粒体参与了大量的细胞过程，即使在细胞呼吸的封闭环境中，线粒体功能这个术语也可以指代多种特征，包括融合与分裂、更新（生物发生和线粒体自噬）以及可塑性。线粒体生物发生，主要是线粒体融合以及线粒体自噬减少，会导致骨关节炎期间出现的代谢紊乱和炎症。MFN2减少和PARKIN表达增加代表了在骨关节炎过程中治疗关节软骨降解的潜在治疗靶点。
