Background and aimsAcute myocardial infarction (AMI) is the most severe coronary heart disease. Left ventricular remodeling occurs and at last results in heart failure after AMI. Left ventricular remodeling is a complex pathophysiology process, including progressive structural, geometric and electrophysiological change, and in which many kinds of cells and cytokines are involved. However, its mechanisms are unclear. Recently, it has been focused on the effects of myocardiocyte apoptosis in left ventricular remodeling after AMI. Bcl-2 family plays an important role in the process of myocardiocyte apoptosis, Bcl-2 protein can inhibit myocardiocyte apoptosis while Bax protein induce myocardiocyte apoptosis. Over-expression of PDCD5 (programmed cell death 5), which has been named TFAR19 (TF-1 cell apoptosis related gene 19), can enhance apoptosis of some cells induced by growth factor withdrawal or serum deprivation and tumor necrosis factor-α (TNF-α), a kind of cytokines, which plays an important role in the process of myocardiocyte apoptosis after AMI. The effects of PDCD5 on left ventricular...
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