Abstract
Purpose: Vascular aetiology of osteoarthritis (OA) has been proposed for decades. However, the exact mechanism remains poorly understood. Endothelin-1 (ET-1) and its type A receptor, originally known for their vasoactivity, have been implicated in OA pathogenesis and management. Very recently, endothelin type B receptor (ETBR) was reported to mediate ET-1-induced endothelial dysfunction via oxidative stress and cellular senescence. In this study, we aimed to determine the role of ET-1/ETBR axis in chondrocyte mitochondria dynamics, reactive oxygen species (ROS) accumulation and cellular senescence in osteoarthritis development.
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