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(Circulation Research. 2009;104:150.)
© 2009 American Heart Association, Inc.

Reviews

Autophagy in Ischemic Heart Disease

Åsa B. Gustafsson, Roberta A. Gottlieb

From the BioScience Center, San Diego State University, Calif.

Correspondence to Roberta Gottlieb, MD, BioScience Center, San Diego State University, 5500 Campanile Dr, San Diego, CA 92182-4650. E-mail robbieg{at}sciences.sdsu.edu

This Review is part of a thematic series on Autophagy, which includes the following articles:

Crosstalk Between Autophagy and Apoptosis in Heart Disease [2008;103:343–351]

Autophagy in Load-Induced Heart Disease [2008;103:1363–1369]

Autophagy in Ischemic Heart Disease

Autophagy in Atherosclerosis: A Cell Survival and Death Phenomenon With Therapeutic Potential
Joseph A. Hill Guest Editor

Autophagy is a major catabolic pathway by which mammalian cells degrade and recycle macromolecules and organelles. It plays a critical role in removing protein aggregates, as well as damaged or excess organelles, to maintain intracellular homeostasis and to keep the cell healthy. In the heart, autophagy occurs at low levels under normal conditions, and defects in this process cause cardiac dysfunction and heart failure. However, this pathway is rapidly upregulated under environmental stress conditions, including ATP depletion, reactive oxygen species, and mitochondrial permeability transition pore opening. Although autophagy is enhanced in various pathophysiological conditions, such as during ischemia and reperfusion, the functional role of increased autophagy is not clear and is currently under intense investigation. In this review, we discuss the evidence for autophagy in the heart in response to ischemia and reperfusion, identify factors that regulate autophagy, and analyze the potential roles autophagy might play in cardiac cells.

Key Words: apoptosis • autophagy • mitochondria • myocardial ischemia

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