Apoptotic and non-apoptotic programmed cardiomyocyte death in ventricular remodelling

Abstract

A defining cellular event in the transition from compensated hypertrophy to dilated cardiomyopathy is cardiomyocyte drop-out due to apoptosis, programmed necrosis, and autophagy. The importance of apoptosis in heart failure has been recognized for over a decade, while other forms of programmed cell death have more recently been appreciated, and their pathophysiological roles continue to be defined in experimental and clinical heart failure. The major focus of this review is on apoptosis in heart failure, with a discussion of molecular cross-talk between apoptosis, autophagy, and programmed necrosis.

Figure 1

Schematic depiction of pathways leading to programmed cardiomyocyte death, as described in the text. Mechanisms of cell death (bottom) are, from left to right, caspase-dependent apoptosis, caspase-independent apoptosis, programmed necrosis, and authophagy. Solid lines show primary effects; interrupted lines depict cross-talk between pathways.