The role of HIF-1α in hypoxic metabolic reprogramming in osteoarthritis . . . Studies have shown that the stability of HIF-1α can stimulate GLS mediated GSH synthesis and reduce ROS production, thereby maintaining redox homeostasis during oxidative or nutritional stress Meanwhile, HIF-1α signaling increases glycogen storage, preventing energy depletion during periods of nutrition or oxygen deprivation [60]
Stabilization of HIF-1α alleviates osteoarthritis via enhancing . . . To explore the mechanism of HIF-1α on mitophagy activation, we investigated the expression HiF-1α BNIP3 classical signaling pathway in the chondrocytes treated with DMOG under hypoxia The BNIP3 expression is necessary for hypoxia-induced autophagy activation and BNIP3 knockdown aggravated cell death during hypoxia 54 , 55