Abstract

Macrophages are essential to the immunological responses associated with atherosclerosis. Recent research on the role of macrophage autophagy (AP) in the development of atherosclerosis has shown a brand-new mechanism by which these cells contribute to vascular inflammation. The transport of cytoplasmic contents to the lysosomal apparatus during AP is a cellular catabolic process that will ultimately result in destruction and recycling. In the early stages of atherosclerosis, basal levels of macrophage AP are crucial for atheroprotection. However, AP deficiency promotes vascular inflammation, oxidative stress, and plaque necrosis in the latter phases of the pathophysiology when it becomes dysfunctional. In this essay, we’ll talk about the involvement of macrophages and AP in atherosclerosis and the growing body of research proving that macrophage AP contributes to vascular disease. We will finally talk on how AP might be targeted for therapeutic utility.