Different types of cell death in vascular diseases.

Abstract

In a mature organism, tissue homeostasis is regulated by cell division and cell demise as the two major physiological procedures. There is increasing evidence that deregulation of these processes is important in the pathogenicity of main diseases, including myocardial infarction, stroke, atherosclerosis, and inflammatory diseases. Therefore, there are ongoing efforts to discover modulating factors of the cell cycle and cell demise planners aiming at shaping innovative therapeutically modalities to the therapy of such diseases. Although the life of a cell is terminated by several modes of action, a few cell deaths exist-some of which resemble apoptosis and/or necrosis, and most of them are different from one another-that contribute to a wide range of functions to either support or disrupt the homoeostasis. Even in normal physiological conditions, cell life is severe within the cardiovascular system. Cells are persistently undergoing stretch, contraction, injurious metabolic byproducts, and hemodynamic forces, and a few of cells sustain decade-long lifetimes. The duration of vascular disease causes further exposure of vascular cells to a novel range of offences, most of which induce cell death. There is growing evidence on consequences of direct damage to a cell, as well as on responses of adjacent and infiltrating cells, which also have an effect on the pathology. In this study, by focusing on different pathways of cell death in different vascular diseases, an attempt is made to open a new perspective on the therapeutic goals associated with cell death in these diseases.