心力衰竭(HF)是以心脏收缩和(或)舒张功能受损为特点的器质性心脏病的终末阶段。在心血管疾病中,HF的发病率和病死率呈不断上升趋势,是一个日趋严重的社会公共难题。HF的发病机理是心肌细胞数目减少(传统解释是细胞死亡),近10年来有大量证据冲击这一传统理论,它们证实细胞凋亡在HF的发生中起到了一定的作用。细胞凋亡是细胞受外环境和细胞内基因调控的一种主动性、程序性死亡形式。许多研究已经把细胞凋亡由“组织特异性”指标变成可延缓HF进展的“治疗目标”。这些研究主要集中在人类与HF的试验模型的临床相关性及抗细胞凋亡治疗的确切疗效方面。 Heart failure (HF) is the terminal stage of organic heart disease characterized by systolic and / or impaired diastolic function. In cardiovascular disease, the incidence of HF and mortality are on the rise, is an increasingly serious social and public problems. The pathogenesis of HF is a decrease in the number of cardiomyocytes (the traditional explanation is cell death). There is a great deal of evidence that this traditional theory has been attacked for nearly 10 years. They confirmed that apoptosis plays a role in the development of HF. Apoptosis is a form of proactive, programmed death in which cells are regulated by both the external environment and intracellular genes. Many studies have turned apoptosis into a “therapeutic target” that delays the progression of HF from a “tissue-specific” indicator. These studies have focused primarily on the clinical relevance of human and HF experimental models and the exact efficacy of anti-apoptotic therapies.