Department of Medicine, Division of Cardiology, University of California San Francisco, San Francisco, California 94143, USA.
J Am Coll Cardiol. 2011 Jan 4;57(1):9-17. doi: 10.1016/j.jacc.2010.08.623.
Aging is a risk factor for heart failure, which is a leading cause of death world-wide. Elderly patients are more likely than young patients to experience a myocardial infarction (MI) and are more likely to develop heart failure following MI. The poor clinical outcome of aging in cardiovascular disease is recapitulated on the cellular level. Increase in stress exposure and shifts in signaling pathways with age change the biology of cardiomyocytes. The progressive accumulation of metabolic waste and damaged organelles in cardiomyocytes blocks the intracellular recycling process of autophagy and increases the cell's propensity toward apoptosis. Additionally, the decreased cardiomyocyte renewal capacity in the elderly, due to reduction in cellular division and impaired stem cell function, leads to further cardiac dysfunction and maladaptive responses to disease or stress. We review the cellular and molecular aspects of post-infarction remodeling in the aged heart, and relate them to the clinical problem of post-infarction remodeling in elderly patients.
衰老是心力衰竭的一个风险因素，心力衰竭是全球范围内的主要死亡原因。老年患者比年轻患者更有可能经历心肌梗死 (MI)，并且在 MI 后更有可能发展为心力衰竭。心血管疾病中衰老的不良临床结果在细胞水平上得到了重现。随着年龄的增长，应激暴露的增加和信号通路的转变改变了心肌细胞的生物学特性。心肌细胞中代谢废物和受损细胞器的逐渐积累会阻断自噬的细胞内循环过程，并增加细胞凋亡的倾向。此外，由于细胞分裂减少和干细胞功能受损，老年人的心肌细胞更新能力下降，导致进一步的心脏功能障碍和对疾病或应激的适应性反应不良。我们回顾了老年心脏梗死后重塑的细胞和分子方面，并将其与老年患者梗死后重塑的临床问题联系起来。
