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Cardiovascular Research 2005 68(3):355-365; doi:10.1016/j.cardiores.2005.08.014
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Copyright © 2005, European Society of Cardiology

Autophagy in cardiac myocyte homeostasis, aging, and pathology

Alexei Termana,* and Ulf T. Brunkb

aDivision of Experimental Pathology, Faculty of Health Sciences, Linköping University, SE-58185, Linköping, Sweden
bDivision of Pharmacology, Faculty of Health Sciences, Linköping University, SE-58185, Linköping, Sweden

* Corresponding author. Tel.: +46 13 221525; fax: +46 13 221529. Email address: alete{at}inr.liu.se

Autophagy, an intralysosomal degradation of cells' own constituents that includes macro-, micro-, and chaperone-mediated autophagy, plays an important role in the renewal of cardiac myocytes. This cell type is represented by long-lived postmitotic cells with very poor (if any) replacement through differentiation of stem cells. Macroautophagy, the most universal form of autophagy, is responsible for the degradation of various macromolecules and organelles including mitochondria and is activated in response to stress, promoting cell survival. This process is also involved in programmed cell death when injury is irreversible. Even under normal conditions, autophagy is somewhat imperfect, underlying gradual accumulation of defective mitochondria and lipofuscin granules within aging cardiac myocytes. Autophagy is involved in the most important cardiac pathologies including myocardial hypertrophy, cardiomyopathies, and ischemic heart disease, a fact that has led to increasing attention to this process.

KEYWORDS Aging; Apoptosis; Cardiomyopathy; Ischemia; Oxygen radicals

Time for primary review 23 days


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