This old heart: Cardiac aging and autophagy

被引:92
|
作者
Linton, Phyllis-Jean [1 ]
Gurney, Michael [1 ]
Sengstock, David [2 ,3 ]
Mentzer, Robert M., Jr. [4 ,5 ,6 ,7 ]
Gottlieb, Roberta A. [6 ,7 ]
机构
[1] San Diego State Univ, Donald P Shiley BioSci Ctr, San Diego, CA 92182 USA
[2] Oakwood Hosp, Div Geriatr Med, Dearborn, MI USA
[3] Wayne State Univ, Sch Med, Dept Internal Med, Detroit, MI 48201 USA
[4] Wayne State Univ, Sch Med, Dept Surg, Cardiovasc Res Inst, Detroit, MI 48201 USA
[5] Wayne State Univ, Sch Med, Dept Physiol, Cardiovasc Res Inst, Detroit, MI 48201 USA
[6] Cedars Sinai Med Ctr, Inst Heart, Los Angeles, CA 90048 USA
[7] Cedars Sinai Med Ctr, Barbra Streisand Womens Heart Ctr, Los Angeles, CA 90048 USA
关键词
Autophagy; Cardiac; Aging; Inflammation; Human studies; CHAPERONE-MEDIATED AUTOPHAGY; INTRACELLULAR REPAIR RESPONSE; AGE-RELATED DECLINE; NLRP3; INFLAMMASOME; OXIDATIVE STRESS; CALORIC RESTRICTION; LIFE-SPAN; ISCHEMIA/REPERFUSION INJURY; DOXORUBICIN CARDIOTOXICITY; MYOCARDIAL-INFARCTION;
D O I
10.1016/j.yjmcc.2014.12.017
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Autophagy, a cellular housekeeping process, is essential to maintain tissue homeostasis, particularly in long-lived cells such as cardiomyocytes. Autophagic activity declines with age and may explain many features of age-related cardiac dysfunction. In this review we summarize the current state of knowledge regarding age-related changes in autophagy in the heart. Recent findings from studies in human hearts are presented, including evidence that the autophagic response is intact in the aged human heart. Impaired autophagic clearance of protein aggregates or deteriorating mitochondria will have multiple consequences including increased arrhythmia risk, decreased contractile function, reduced tolerance to ischemic stress, and increased inflammation; thus autophagy represents a potentially important therapeutic target to mitigate the cardiac consequences of aging. This article is part of a Special Issue entitled CV Aging. (C) 2014 The Authors. Published by Elsevier Ltd.
引用
收藏
页码:44 / 54
页数:11
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