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In the condition of hypoxia and ischemia/reperfusion, hyperphosphorylation of COX subunit I, IV, and V (COX1, COX2, and COX5) inhibited COX activity, resulting in an increase of ROS production ( 2+ accumulation by the action of mitochondrial Ca 2+ uniporter (MCU) ( 2+ accumulation and ROS production resulted in the sustained opening of permeability transition pore complex followed by the mitochondrial permeability transition (MPT), inflammation and cell/tissue damages in ischemic hearts ( In mitochondria, a family of Bcl-related proteins, including both anti-apoptotic (Bcl-2, Bcl-xL) and pro-apoptotic (Bad, Bak, Bax) members, involves in initiated apoptosis

With rising global incidence and expanding patient populations, the therapeutic landscape for T2D has evolved rapidly

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