Wu Longhuo, Liu Haiqing, Li Linfu, Liu Hai, Cheng Qilai, Li Hongliang, Huang Hao
College of Pharmacy, Gannan Medical University, Ganzhou 341000, China.
Curr Drug Targets. 2014;15(7):710-9. doi: 10.2174/1389450115666140417120305.
Osteoarthritis (OA) is a chronic degenerative disease leading to aberrance of cartilage structures with unclear or multifactorial mechanisms. Recently, a great portion of research endeavor to explore the molecular mechanisms of OA in focusing on the mitochondrial pathology. Mitochondrial respiratory chain (MRC) produces reactive oxygen species (ROS), which in turn impair mtDNA integrity and link to cartilage degradation in OA. The fine-tuning between ROS and antioxidant within chondrocytes ensures cartilage homeostasis. With disturbance from pro-inflammatory cytokines, oxidative stress synergistically instigates cellular signaling and exacerbates mitochondrial pathology, which may affect several pathways implicated in OA cartilage degradation, including oxidative stress, increase of cytokine-induced chondrocytes inflammation and matrix catabolism, aging and senescence, obesity-related pathology, and cartilage matrix calcification. Unveiling the molecular mechanisms of mitochondrial function in OA pathogenesis and progression is essential for providing relevant therapeutic targets. These suggest that efficient protection and improvement of mitochondrial activity can be a therapeutic alternative for OA patients.
骨关节炎（OA）是一种慢性退行性疾病，其导致软骨结构异常，发病机制不明或为多因素所致。近来，大量研究致力于探索骨关节炎的分子机制，重点关注线粒体病理学。线粒体呼吸链（MRC）产生活性氧（ROS），进而损害线粒体DNA完整性，并与骨关节炎中的软骨降解相关。软骨细胞内ROS与抗氧化剂之间的精细调节确保了软骨的稳态。在促炎细胞因子的干扰下，氧化应激协同激活细胞信号传导并加剧线粒体病理学变化，这可能影响与骨关节炎软骨降解相关的多种途径，包括氧化应激、细胞因子诱导的软骨细胞炎症增加和基质分解代谢、衰老和老化、肥胖相关病理学以及软骨基质钙化。揭示线粒体功能在骨关节炎发病机制和进展中的分子机制对于提供相关治疗靶点至关重要。这些表明，有效保护和改善线粒体活性可能是骨关节炎患者的一种治疗选择。
