Molecular Mechanisms of Apoptosis in Heart Failure

One of the most compelling issues to impact on contemporary cardiology to date is undoubtedly the concept of apoptosis or programmed cell death. Apoptosis, while crucial for normal embryonic development has been implicated in the pathogenesis of a number of cardiac pathologies including ischemia, oxidative stress injury, infarction and more recently heart failure. The loss of functional cardiac myocytes through activation of an apoptotic program may ultimately contribute to ventricular remodeling and the demise of ventricular function incompatible with the body's needs. The molecular mechanisms that underlie cardiac cell apoptosis remain poorly defined, however, there is increasing awareness that external as well as internal factors such tumor suppressor protein p53, cytokines including TNFα and mitochondria are potential triggers of cardiac apoptosis. Therefore, a better understanding of the role played by these factors would facilitate the advent of therapeutic agents to modulate inappropriate cardiac cell loss as a means to preserve cardiac function and prevent heart failure.