ABSTRACT
Apoptosis is a highly regulated form of cell death that acts as the essential counterpart of cell proliferation.1
Initially described in the context of organ morphogenesis in the invertebrate nematode and mammalian embryo, apoptosis is often referred to as ‘programmed cell death’. For instance, an increase in programmed cell death of cardiomyocytes in the right ventricle has been implicated in normal assymetrical postnatal morphogenesis of the cardiac chambers.2 The identification over the last 15 years of the key genes mediating apoptotic cell death in mammalians has set the stage for a remarkable increase in studies implicating apoptosis in cardiovascular diseases. As discussed below, these include conditions where apoptosis is increased relative to cell replication, such as in cardiomyocyte loss during progression to heart failure, arterial atrophy leading to aneurysm, and capillary rarefaction in hypertension. In contrast, decreased apoptosis relative to cell replication can lead to tissue hyperplasia, as in arterial remodeling in hypertension and atherosclerosis. Finally, enhanced cell turnover due to an increase in both apoptosis and cell proliferation has been proposed as a mechanism leading to premature endothelial cell senescence.
