Is autophagy a double-edged sword for the heart?
Autophagy is a catabolic process through which damaged or long-lived proteins, macromolecules and organelles are degraded using lysosomal degradative machinery. Since cardiac myocytes are terminally differentiated, the role of autophagy is essential to maintain the homeostasis of the myocardium. Autophagy supplies nutrients for the synthesis of essential proteins during starvation and thus helps to extend cell survival. Although autophagy is non-selective, under oxidative conditions it effectively removes oxidatively damaged mitochondria, peroxisomes and endoplasmic reticulum. Thus, autophagy can protect the cells from apoptosis and other major injuries, and it is considered to be in the cross-road between cell death and survival. However, excess autophagy can destroy essential cellular components and lead to cell death. The function of autophagy in normal and in the conditions of cardiac diseases such as heart failure, cardiomyopathy, cardiac hypertrophy, and ischemia-reperfusion injury is discussed.
Gurusamy
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N
School of Medicine, Cardiovascular Research Center, University of Connecticut, Farmington, CT 06030-1110, USA.
Das
Dipak K
DK
D000818:Animals; D001343:Autophagy; D002470:Cell Survival; D006331:Heart Diseases / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D009206:Myocardium / Q000378:metabolism / Q000473:pathology*; D018384:Oxidative Stress; D015398:Signal Transduction