Mitochondria as a Therapeutic Target in Heart Failure

被引：262

作者：

Bayeva, Marina ^{[1
]}

Gheorghiade, Mihai ^{[2
]}

Ardehali, Hossein ^{[1
]}

机构：

[1] Northwestern Univ, Sch Med, Feinberg Cardiovasc Res Inst, Chicago, IL 60611 USA

[2] Northwestern Univ, Sch Med, Ctr Cardiovasc Innovat, Chicago, IL 60611 USA

来源：

JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY | 2013年 / 61卷 / 06期

基金：

美国国家卫生研究院;

关键词：

cardiomyocytes; heart failure; mitochondria; ACTIVATED PROTEIN-KINASE; ISCHEMIA-REPERFUSION INJURY; PERMEABLE PEPTIDE ANTIOXIDANTS; INDUCED CARDIAC-HYPERTROPHY; NITRIC-OXIDE SYNTHASE; MYOCARDIAL-INFARCTION; PRESSURE-OVERLOAD; OXIDATIVE STRESS; FRIEDREICHS-ATAXIA; REACTIVE OXYGEN;

D O I：

10.1016/j.jacc.2012.08.1021

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Heart failure is a pressing public health problem with no curative treatment currently available. The existing therapies provide symptomatic relief, but are unable to reverse molecular changes that occur in cardiomyocytes. The mechanisms of heart failure are complex and multiple, but mitochondrial dysfunction appears to be a critical factor in the development of this disease. Thus, it is important to focus research efforts on targeting mitochondrial dysfunction in the failing heart to revive the myocardium and its contractile function. This review highlights the 3 promising areas for the development of heart failure therapies, including mitochondrial biogenesis, mitochondrial oxidative stress, and mitochondrial iron handling. Moreover, the translational potential of compounds targeting these pathways is discussed. (J Am Coll Cardiol 2013;61:599-610) (C) 2013 by the American College of Cardiology Foundation

引用

页码：599 / 610

页数：12

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