Cell-specific role of apoptosis in the process of atherosclerosis

Atherosclerosis is a chronic disease of the arterial wall characterized by the accumulation of fatty and fibrous material in the intima. It is the primary cause of cardiovascular disease, which is associated with high mortality and morbidity rates, particularly in aging populations. Apoptosis is a tightly regulated form of programmed cell death that eliminates unneeded or harmful cells. Its role in the process of atherosclerosis has been the subject of numerous recent studies. In this context, the impact of apoptosis on atherosclerosis was comprehensively examined through a narrative literature review. The effect of apoptosis on atherosclerosis depends on the cell types involved and the stage of the disease. Endothelial cell apoptosis, exacerbated by aging, may disrupt the integrity of the vascular lining and thereby facilitate the infiltration of lipids into the subendothelial space and promote plaque vulnerability. Evidence suggests that apoptosis of vascular smooth muscle cells can inhibit their migration and proliferation and attenuate plaque formation in early atherosclerosis but also induce plaque instability by thinning the fibrous cap in the advanced stages of the disease. Macrophage apoptosis plays a dual role in atherosclerosis depending on its timing as it can limit lesion cellularity and suppress plaque progression in the initial stages while exacerbating necrotic core development and plaque vulnerability in the late stages. Although more studies are required to fully elucidate the role of apoptosis in atherosclerosis, its therapeutic manipulation appears to be a promising strategy for addressing this multifactorial disease.