Abstract
Atherosclerosis is a chronic progressive condition in which the wall of the artery develops abnormalities and causes thickening of the blood vessels. The development of atherosclerosis is a complex process characterized by vascular inflammation and the growth of atherosclerotic plaques that eventually lead to compromised blood flow. The endothelial to mesenchymal transition (EndMT) is a phenomenon whereby endothelial cells lose their endothelial properties and acquire a mesenchymal phenotype similar to myofibroblast and smooth muscle cells. This process is considered a key contributor to the development and, importantly, the progression of atherosclerosis. Thus, therapeutically targeting the EndMT will provide a broad strategy to attenuate the development of atherosclerosis. Here, we review our current knowledge of EndMT in atherosclerosis including several key pathways such as hypoxia, TGF-β signaling, inflammation, and environmental factors during the development of atherosclerosis. In addition, we discuss several transgenic mouse models for studying atherosclerosis. Taken together, rapidly accelerating knowledge and continued studies promise further progress in preventing this common chronic disease.
Highlights
Atherosclerosis is a major cause of mortality and morbidity worldwide with clinical outcomes such as ischemic heart disease, ischemic stroke, renal ischemia, and peripheral vascular disease
Therapies targeting endothelial to mesenchymal transition (EndMT), including the signaling pathways, could provide an avenue to ameliorate the development of atherosclerosis
The Transforming growth factor β feature (TGF-β) and fibroblast growth factors (FGFs) signaling pathways can be harnessed as potential targets; care should be taken as they are involved in multiple processes in cells that could have unwarranted effects
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Atherosclerotic plaques narrow the lumen of vessels, obstructing blood flow, making organs susceptible to ischemia; plaques may rupture, leading to adverse effects such as myocardial ischemia or infarction, renal ischemia, and ischemic stroke due to the activated endothelial and smooth muscle cells, macrophages, lymphocytes, and large amounts of extracellular matrix during the process [14,15,16]. The EndMT process has been reported to be associated with additional pathophysiological processes in cardiovascular-related diseases, including atherosclerosis [21,22]. During this process, the endothelial cells lose their apical-to-basal membrane polarity and cell-to-cell adhesion and acquire a migratory, fibroblast-like phenotype.
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