Abstract
Cardiovascular complications are associated with advanced atherosclerosis. Although atherosclerosis is still regarded as an incurable disease, at least in its more advanced stages, the discovery of endothelial progenitor cells (EPCs), with their ability to replace old and injured cells and differentiate into healthy and functional mature endothelial cells, has shifted our view of atherosclerosis as an incurable disease, and merged traditional theories of atherosclerosis pathogenesis with evolving concepts of vascular biology. EPC alterations are involved in the pathogenesis of vascular abnormalities in atherosclerosis, but many questions remain unanswered. Many currently available drugs that impact cardiovascular morbidity and mortality have shown a positive effect on EPC biology. This review examines the role of endothelial progenitor cells in atherosclerosis development, and the impact standard antilipemic drugs, including statins, fibrates, and ezetimibe, as well as more novel treatments such as proprotein convertase subtilisin/kexin type 9 (PCSK9) modulating agents and angiopoietin-like proteins (Angtpl3) inhibitors have on EPC biology.
Highlights
Atherosclerosis is a vascular disease caused by the build-up of plaques in the innermost layers of arteries, leading to arterial wall thickening and hardening, and narrowing of the arterial lumina [1]
This review examines the role of endothelial progenitor cells in atherosclerosis development, and the impact standard antilipemic drugs, including statins, fibrates, and ezetimibe, as well as more novel treatments such as proprotein convertase subtilisin/kexin type 9 (PCSK9) modulating agents and angiopoietin-like proteins (Angtpl3) inhibitors have on EPC biology
This review focuses on the role of endothelial progenitor cells in atherosclerosis, and the impact standard as well as novel lipid-lowering treatments have on EPC-related vascular repair
Summary
Atherosclerosis is a vascular disease caused by the build-up of plaques in the innermost layers of arteries, leading to arterial wall thickening and hardening, and narrowing of the arterial lumina [1]. Fibrous caps may rupture, exposing the underlying extremely thrombogenic core Such events prompt further thrombus formation and release of more inflammatory mediators, resulting in arterial stenosis or occlusion [1]. This leads to end organ damage, and depending on the anatomic site of the injured vessel, presents as myocardial infarction, ischemic stroke, or critical limb ischemia [5–7]. Due to the unique characteristics of these cell lines, the idea that atherosclerosis regression was possible emerged These myeloid derived cells are capable of virtually endless division and differentiation into healthy and functional endothelial cells at the site of vessel injury, repairing the vessel wall, and promoting neovascularization [9,10]. This review focuses on the role of endothelial progenitor cells in atherosclerosis, and the impact standard as well as novel lipid-lowering treatments have on EPC-related vascular repair
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