Autophagy, Myocardial Protection, and the Metabolic Syndrome

被引：69

作者：

Giricz, Zoltan ^{[1
]}

Mentzer, Robert M., Jr. ^{[1
,2
,3
]}

Gottlieb, Roberta A. ^{[1
]}

机构：

[1] San Diego State Univ, Donald P Shiley BioSci Ctr, Dept Biol, San Diego, CA 92182 USA

[2] Wayne State Univ, Sch Med, Dept Physiol, Cardiovasc Res Inst, Detroit, MI 48201 USA

[3] Wayne State Univ, Sch Med, Dept Surg, Detroit, MI 48201 USA

来源：

JOURNAL OF CARDIOVASCULAR PHARMACOLOGY | 2012年 / 60卷 / 02期

关键词：

autophagy; cardioprotection; metabolic syndrome; myocardial ischemia and reperfusion; ACTIVATED PROTEIN-KINASE; ISCHEMIA-REPERFUSION INJURY; TERM CALORIC RESTRICTION; OXIDATIVE STRESS; DIABETIC HEART; ISCHEMIA/REPERFUSION INJURY; MITOCHONDRIAL DYSFUNCTION; ROSIGLITAZONE TREATMENT; DIFFERENTIAL ROLES; INSULIN-RESISTANCE;

D O I：

10.1097/FJC.0b013e318256ce10

中图分类号：

R5 [内科学];

学科分类号：

100201 [内科学];

摘要：

Autophagy is a housekeeping process that helps to maintain cellular energy homeostasis and remove damaged organelles. In the heart, autophagy is an adaptive process that is activated in response to stress including acute and chronic ischemia. Given the evidence that autophagy is suppressed in energy-rich conditions, the objective of this review is to examine autophagy and cardioprotection in the setting of the metabolic syndrome. Clinical approaches that involve the induction of cardiac autophagy pharmacologically to enhance the heart's tolerance to ischemia are also discussed.

引用

页码：125 / 132

页数：8

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