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Decreased mitochondrial energy metabolism during cardiac ischemia could be restored following reperfusion, but the early mitochondrial calcium overload and excessive ROS production boost the opening of mitochondrial permeability transition pore (mPTP) and depolarization of mitochondrial membrane potential (MMP), ultimately leading to cell apoptosis ( in vitro study, SA pretreatment inhibited mitochondrial apoptosis pathway involving mPTP opening, loss of transmembrane potential (m), and cleavage of mitochondrial apoptosis-related proteins (caspase-9 and caspase-3) ( in vitro or ex vivo studies offer valuable insights into SA-related regulations via targeting mitochondria in MIRI, but future in vivo investigations are still needed to confirm these findings