Murriel Christopher L, Mochly-Rosen Daria
Department of Molecular Pharmacology, Stanford University School of Medicine, Stanford, CA 94305-5174, USA.
Arch Biochem Biophys. 2003 Dec 15;420(2):246-54. doi: 10.1016/j.abb.2003.08.038.
Heart attacks, or acute myocardial infarctions (AMI), affect more than one million people in the US every year. The damage that occurs to the heart by AMI is often permanent and as a result, the morbidity and mortality rates of patients that experience AMIs continue to be high. Consequently, AMI patients are at significantly increased risks for future myocardial infarctions, decreased heart function, heart failure, and death [Heart and Stroke statistical update. In American Heart Association (2002) 4]. In this review, we discuss the events that lead to cardiac damage by AMI. Specifically, we discuss the current understanding of the role of ischemic damage vs. reperfusion damage, which is induced by the return of blood, oxygen, and nutrients to the organ. We also discuss the role of apoptosis and necrosis in cardiac damage, the means to protect the heart from damage by ischemia and reperfusion, and the role of protein kinase C in these processes.
心脏病发作,即急性心肌梗死(AMI),在美国每年影响超过100万人。急性心肌梗死对心脏造成的损害往往是永久性的,因此,经历过急性心肌梗死的患者的发病率和死亡率仍然很高。因此,急性心肌梗死患者未来发生心肌梗死、心脏功能下降、心力衰竭和死亡的风险显著增加[《心脏与中风统计更新》。美国心脏协会(2002年)4]。在本综述中,我们讨论导致急性心肌梗死引起心脏损害的事件。具体而言,我们讨论了目前对缺血性损伤与再灌注损伤作用的理解,再灌注损伤是由血液、氧气和营养物质回流到器官所诱发的。我们还讨论了细胞凋亡和坏死在心脏损伤中的作用、保护心脏免受缺血和再灌注损伤的方法以及蛋白激酶C在这些过程中的作用。