Cardiovascular diseases: Altering apoptosis for a healthy heart

Abstract Cardiovascular diseases are the leading cause of morbidity and mortality in developing as well as developed nations. Apoptosis which is also called programmed cell death is a highly regulated process and plays a vital role during cardiovascular development, including the development of the embryonic outflow tract, cardiac valves, conducting system, and coronary vasculature. Moreover, in several pathologic conditions like ischemic heart disease reperfusion injury, acute and chronic myocardial infarction, cardiomyopathy as well as in case of acute and chronic heart failure, apoptosis is significantly involved. Apoptosis plays an essential role in the pathogenesis of ischemia/reperfusion where prolonged ischemia leads to increased necrosis, while reperfusion is responsible for increased apoptosis. Although during heart failure there is a modest increase in apoptosis of cardiomyocytes, apoptosis seems to play an important role in the pathogenesis of heart failure. Although adult cardiomyocytes are postmitotic cells has decreased capacity to proliferate and respond to regenerative signals when compared to infants and pediatrics and has limited response capability for regeneration and repair still the input of apoptosis over time from years proves a significant clinical factor in the pathogenesis of heart failure. Myocardial infarction and heart failure are complex cellular processes and cell death plays a critical role in the pathogenesis of both syndromes. The regulated nature of cell death in these diseases opens the possibility of manipulating death pathways to therapeutic advantage. Indeed, the inhibition of cardiac apoptosis holds promise as an effective therapeutic strategy for the management of cardiovascular diseases.