Apoptosis and vascular wall remodeling in hypertension

Vascular structure plays a key role in the pathogenesis of hypertension. Because it is less readily reversible than protein accumulation, DNA accumulation in the arterial wall may be considered as a record of past episodes of vascular growth, contributing to the persistence of the vascular disease. Apoptosis, a ubiquitous and highly regulated form of programmed cell death that is involved in tissue morphogenesis and homeostasis as the essential counterpart of cell replication, is potentially involved in the regulation of vascular structure, via the deletion of cells in the vessel wall. We discuss how the current knowledge on apoptosis may provide insights into the pathogenesis of vascular wall remodeling, with an emphasis on the biology of vascular smooth muscle cells. Evidence suggests that heightened cell replication rates are often associated with increased apoptosis, as for smooth muscle cells in genetic hypertension or in arterial repair after injury. However, apoptotic cell death may also be regulated independently of cell growth. The triggering of apoptosis depends on a balance of environmental cues that are not specific to apoptosis. However, there is a common set of key biochemical events mediating apoptosis (i.e., committing the cell to die), thus providing a basis for the design of novel pharmacological strategies specifically targeting apoptotic cell death. The identification of biochemical markers of apoptosis and other methodological advances will ultimately help in understanding the role of apoptotic cell death in vascular remodeling and hypertensive end-organ damage.