Abstract
Cartilage destruction is central in the pathogenesis of osteoarthritis (OA), an age-related chronic degenerative disease. Cartilage degeneration has been postulated to occur due to chondrocyte senescence. On the other hand, type 2 diabetes mellitus (T2DM) is an independent risk factor for OA initiation and progression, bringing about the concept of “diabetic OA (DM-OA).” Aberrant metabolic pathways in T2DM promote a chronic inflammatory environment that favors cell apoptosis and senescence. However, it is still unclear if the cartilage of diabetic OA patients contains a higher amount of senescent chondrocytes compared to nondiabetic patients.
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