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.
Keywords: Aging, chondrocytes, leptin, mitochondrial pathology, obesity, osteoarthritis, pro-inflammatory cytokines, ROS.
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