MacLellan W R, Schneider M D
Molecular Cardiology Unit, Baylor College of Medicine, Houston, Tex 77030, USA.
Circ Res. 1997 Aug;81(2):137-44. doi: 10.1161/01.res.81.2.137.
Programmed cell death (apoptosis) is recognized, increasingly, as a contributing cause of cardiac myocyte loss with ischemia/reperfusion injury, myocardial infarction, and long-standing heart failure. Although the exact mechanisms initiating apoptosis in these in vivo settings remain unproven, insights into the molecular circuitry controlling apoptosis more widely suggest the potential to protect mammalian ventricular muscle from apoptosis through one or more of these pathways, by pharmacological means or, conceivably, gene transfer.
程序性细胞死亡(凋亡)越来越被认为是导致心肌细胞因缺血/再灌注损伤、心肌梗死和长期心力衰竭而丧失的一个原因。尽管在这些体内情况下启动凋亡的确切机制尚未得到证实,但对更广泛控制凋亡的分子机制的深入了解表明,有可能通过药理手段或可以想象的基因转移,通过这些途径中的一种或多种来保护哺乳动物心室肌免受凋亡。