Abstract
Heart failure (HF) has become the dominant cardiovascular disorder in the Western world and Japan, so there is an urgent need to clarify the mechanisms governing pathological remodeling mediated through cell death, and to identify ways of preventing and treating HF. Historically, there are 3 types of cell death: apoptosis, autophagy and necrosis. Apoptosis, a form of programmed cell death, has been well characterized and the molecular events involved in apoptotic death are well understood. Necrosis is often defined in a negative manner: death lacking the characteristics of programmed cell death and thus accidental and uncontrolled. However, recent studies indicate that necrosis is tightly regulated. Autophagy is a cell survival mechanism that involves degradation and recycling of cytoplasmic components. In contrast to the other 2 mechanisms, autophagy may mediate cell death under specific circumstances. In fact, damaged cardiomyocytes that show characteristics of autophagy have been observed during HF. However, a recent study indicated that upregulation of autophagy in the failing heart is an adaptive response. This review summarizes recent findings regarding the molecular mechanisms of cardiomyocyte cell death in HF.
