Dorn Gerald W
Center for Pharmacogenomics and Cardiovascular Division, Department of Internal Medicine, Washington University, 660 S. Euclid Ave., Campus Box 8086, St Louis, MO 63110, USA.
Cardiovasc Res. 2009 Feb 15;81(3):465-73. doi: 10.1093/cvr/cvn243. Epub 2008 Sep 8.
A defining cellular event in the transition from compensated hypertrophy to dilated cardiomyopathy is cardiomyocyte drop-out due to apoptosis, programmed necrosis, and autophagy. The importance of apoptosis in heart failure has been recognized for over a decade, while other forms of programmed cell death have more recently been appreciated, and their pathophysiological roles continue to be defined in experimental and clinical heart failure. The major focus of this review is on apoptosis in heart failure, with a discussion of molecular cross-talk between apoptosis, autophagy, and programmed necrosis.
从代偿性肥大转变为扩张型心肌病过程中的一个决定性细胞事件是由于凋亡、程序性坏死和自噬导致的心肌细胞丢失。凋亡在心力衰竭中的重要性在十多年前就已得到认可,而其他形式的程序性细胞死亡最近才受到关注,它们在实验性和临床心力衰竭中的病理生理作用仍在不断明确。本综述的主要重点是心力衰竭中的凋亡,并讨论凋亡、自噬和程序性坏死之间的分子相互作用。