Mitochondria are critical regulators of cell function and cellular survival. Many lines of evidence suggest that mitochondria have a central role in ageing-related diseases. Mutations in mitochondrial DNA and oxidative stress both contribute to ageing. Osteoarthritis (OA) is a rheumatic disease associated to aging and it is characterized by articular cartilage degradation and increases of chondrocyte death. Articular cartilage chondrocytes must survive and maintain tissue integrity in an avascular environment. Then chondrocytes from deep and superficial zones may require adaptively increased anaerobic glucolysis and aerobic respiration respectively to support ATP synthesis. Recent ex vivo studie reported dysfunction of mitochondrial human OA chondrocytes. The analysis of mitochondrial electron transport chain activity in OA chondrocytes shows a significant decrease in Complexes I, II and III compared to normal chondrocytes. This mitochondrial dysfunction can mediate several pathways implicated in cartilage degradation such as, oxidative stress, inadequacy of chondrocyte biosynthetic and growth responses, up-regulated chondrocyte cytokine-induced inflammation and matrix catabolism, pathologic cartilage matrix calcification and increased chondrocyte death (necrosis or apoptosis). Mitochondrial dysfunction in OA chondrocytes may be originated by somatic mutations in mtDNA or by direct effect of pro-inflammatory mediators (cytokines, prostaglandin, ROS and NO) on mitochondrial activity.
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