Mani Kartik
Cardiovascular Research Center, Albert Einstein College of Medicine, Golding G-01, Morris Park Av., Bronx, NY 10461, USA.
Heart Fail Rev. 2008 Jun;13(2):193-209. doi: 10.1007/s10741-007-9073-7.
The most common cause of systolic dysfunction in the United States is prior ischemic injury. As the basic functional unit of the myocardium, the cardiac myocyte is the ultimate target of both the pathogenesis and possible therapies in this paradigm. Maintaining adequate numbers of these terminally differentiated units in the myocardium has been the focus of all therapies in ischemic syndromes, including reperfusion strategies. Programmed cell death, in the forms of apoptosis, necrosis and possibly, autophagic cell death are the final arbiters of myocyte numbers following myocardial infarction. This review will focus on the evidence for cell death in the development of heart failure following myocardial infarction, a brief review of the relevant pathways and the targets for development of future therapies.
在美国，收缩功能障碍最常见的原因是既往缺血性损伤。作为心肌的基本功能单位，心肌细胞是这种范例中发病机制和可能治疗方法的最终靶点。在心肌中维持足够数量的这些终末分化细胞一直是缺血综合征所有治疗方法的重点，包括再灌注策略。以凋亡、坏死以及可能的自噬性细胞死亡形式出现的程序性细胞死亡是心肌梗死后心肌细胞数量的最终决定因素。本综述将聚焦于心肌梗死后心力衰竭发展过程中细胞死亡的证据、相关途径的简要回顾以及未来治疗方法开发的靶点。
