Cell senescence is defined as irreversible cell cycle arrest characterized by significant alterations in gene and protein expression and the production of senesence-associated secretory phenotype.A severe imbalance between blood flow demand and supply in the myocardium after myocardial infarction can lead to the occurrence of stress-induced premature senescence,which plays an important role in determining cardiac function outcomes after myocardial infarction.This article mainly reviews the role and mechanism of stress-induced premature senescence in maintaining cardiac function in myocardial infarction,as well as the effect of drugs developed for cell senescence on cardiac function after myocardial infarction,so as to provide some new ideas for the treatment of myocardial infarction by regulating cellular senescence.
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