Autophagy in the myocardium: Dying for survival?

Autophagy is an intracellular phenomenon in which a cell digests its own constituents. Autophagy is well conserved in nature from lower eukaryotes to mammals and has been attributed to disparate physio-logical events – including cell death, the mechanism of which is dif-ferent from apoptosis. However, unlike in apoptosis, in which a family of cysteine proteases (caspases) and a number of other regula-tory proteins have been identified and characterized, the mechanism of autophagic cell death remains unclear. In addition, the general mechanisms by which autophagy is initiated and modulated are just emerging, and several lines of evidence indicate that activated class I phosphatidylinositol 3-kinase and mammalian target of rapamycin (mTOR) inhibit autophagy, while class III phosphatidylinositol 3-kinase acts as a facilitator. Autophagy has been attributed to a number of cardiac disorders, such as ischemic cardiomyopathy, car-diac hypertrophy, hemochromatosis and myocardial aging. Inductio