摘要Acute myocardial infarction-induced cardiogenic shock(AMI-CS)is a severe cardio-vascular emergency that often occurs after acute myocardial infarction(AMI).The main characteristic of AMI-CS is a sharp decline in the heart's pumping function,leading to inadequate blood and oxygen supply to systemic tissues and organs,which in turn induces multi-organ failure.In recent years,in-creasing evidence has shown that mitochondria-mediated apoptosis plays a crucial role in the patho-physiological process of AMI-CS.Mitochondrial fission,regulated by proteins such as dynamin-relat-ed protein 1(Drp1)and mitochondrial fission factor(Mff),is a critical event during apoptosis.This process leads to mitochondrial fragmentation,loss of mitochondrial membrane potential,and in-creased production of mitochondrial reactive oxygen species(mROS).These changes result in cardio-lipin oxidation and the dissociation of hexokinase 2(HK2)from voltage-dependent anion channel 1(VDAC1),facilitating the release of cytochrome c and subsequent activation of the apoptotic cascade.This review delves into the molecular mechanisms underlying mitochondrial fission and its regulation,emphasizing recent findings on the interplay between mitochondrial dynamics and apoptosis.Further-more,it explores potential therapeutic strategies targeting mitochondrial fission and apoptosis to miti-gate the detrimental effects of AMI-CS,highlighting promising avenues for future research and clinical intervention.