Recent Advances: From Cell Biology to Cell Therapy in Atherosclerosis Plaque via Stent Implantation

Abstract

Atherosclerosis is a multifactorial result of complicated pathophysiology. Changes in the expression of polygenes, coupled with environmental and lifestyle factors, trigger a cascade of adverse events involving a variety of cell types, such as vascular endothelial cells, smooth muscle cells, and macrophages. In this review, we summarize the function and therapeutic targets of atherosclerotic cells. This article reviews the role of endothelial cells, smooth muscle cells, macrophages and foam cells in the development of atherosclerosis and the progress in the treatment of atherosclerosis by targeting these cells. Atherosclerotic plaque involves a variety of cells and biomolecules, and its complex biological environment is a difficult point for the study and treatment of atherosclerosis. For treating atherosclerosis, a large number of studies emerged based on blocking or inhibiting factors affecting the formation and development of plaque. Cardiovascular stent intervention is currently the main method for the treatment of atherosclerosis. In recent decades, numerous studies on cardiovascular, stents mainly involve drug coating or biomolecular modification of stents to enhance anti-thrombosis, anti-restenosis and endothelialization. This paper introduces the research status of cardiovascular stents and new strategies for surface modification. The treatment of atherosclerosis based on the level of molecular biology and cell biology is becoming a research hotspot in the coming decades.

Contrast-Enhanced Ultrasound Feasibility in Assessing Carotid Plaque Vulnerability—Narrative Review

“…Plaque vulnerability is a factor that should be at the center of interest for every sonographer because it has a direct impact on the patient's risk of a stroke [57]. The proper assessment of plaque instability should include the thickness of the fibrous cap, the size of the lipid-necrotic nucleus, ascertaining the presence of plaque neovascularization, determining the direction of atherosclerotic plaque remodeling, and ascertaining the presence of ulceration [58,59]. Vulnerability also defines the type of recommended treatment; it should be conservative in the case of stable plaques or interventional when it comes to unstable, ulcerated plaques [60].…”