摘要
乙醇(酒精)对心血管系统有多重影响,长期酗酒会引起明显的心脏毒性效应,乙醇及其代谢产物可能引发酒精性心肌病,甚至导致猝死.这种毒性作用可能与多种机制有关,包括线粒体功能缺陷、氧化应激损伤、蛋白质合成受损及分解代谢异常、脂肪酸代谢紊乱等.这些机制相互作用,最终导致细胞的死亡.细胞死亡是乙醇导致心肌损伤和功能障碍的重要机制之一,在急、慢性酒精动物模型和酒精性心肌病患者心脏标本中得到验证.本文通过对乙醇致心肌损伤过程中发生的凋亡、自噬、铁死亡、坏死性凋亡、焦亡等多种细胞死亡方式的分子作用机制进行阐述和归纳总结,旨在进一步探讨酒精性心脏损害的发病机制,以期为酒精摄入所致的心脏损害提供一些新的干预靶点和治疗方案.
Abstract
Ethanol(alcohol)has multiple effects on the cardiovascular system,long-term alcohol abuse can cause sig-nificant cardiotoxic effects,ethanol and its metabolites may trigger alcoholic cardiomyopathy,and even lead to sudden death.This toxic effect may be related to a variety of mechanisms,including mitochondrial dysfunction,oxidative stress in-jury,protein synthesis impairment,catabolism abnormalities,fatty acid metabolism disorders,etc.These mechanisms in-teract and ultimately lead to cell death.Cell death is one of the important mechanisms of myocardial injury and dysfunction caused by alcohol,which has been verified in acute and chronic alcohol animal models and cardiac specimens of alcoholic cardiomyopathy patients.This paper elaborated and summarized the molecular mechanisms of apoptosis,autophagy,iron death,necrotic apoptosis,pyrodeath and other cell death modes in the process of alcohol-induced myocardial injury,aim-ing to further explore the pathogenesis of alcohol-induced heart damage,in order to provide some new intervention targets and treatment plans for alcohol-induced heart damage.
NETL
NSTL
维普
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