Andréka P, Müzes G, Nádházi Z
II. Belgyógyászati Klinika, Semmelweis Orvostudományi Egyetem, Budapest.
Orv Hetil. 1999 Jan 17;140(3):135-42.
Heart failure can result from a variety of causes, including volume or pressure overload and contractile disturbances of the myocardium. Loss of myocytes is an important mechanism in the development of cardiac failure. In general, myocyte death resulting in progressive deterioration of myocardial function is attributed to necrosis, but recently the involvement of programmed cell death (mainly apoptosis) has been suggested. The authors review the possible role of myocardial apoptosis in developing of heart failure. Subcellular genetic regulatory processes as well as the pharmacological susceptibility of programmed cell death are also discussed. In heart failure, significant amount of cardiac myocytes undergoes apoptosis, that unlike necrosis can be prevented. Specific inhibition of this process could mean a considerable part of cardioprotection after thorough understanding of the underlying cellular mechanisms.
心力衰竭可由多种原因引起,包括容量或压力负荷过重以及心肌收缩功能障碍。心肌细胞丢失是心力衰竭发生发展的重要机制。一般来说,导致心肌功能逐渐恶化的心肌细胞死亡归因于坏死,但最近有人提出程序性细胞死亡(主要是凋亡)也参与其中。作者综述了心肌凋亡在心力衰竭发生中的可能作用。还讨论了亚细胞遗传调控过程以及程序性细胞死亡的药物敏感性。在心力衰竭中,大量心肌细胞发生凋亡,与坏死不同,凋亡是可以预防的。在深入了解潜在细胞机制后,特异性抑制这一过程可能意味着相当一部分的心脏保护作用。