Role of vascular smooth muscle cell in the inflammation of atherosclerosis

Abstract

Atherosclerosis is a pathologic process occurring within the artery, in which many cell types, including T cell, macrophages, endothelial cells, and smooth muscle cells, interact, and cause chronic inflammation, in response to various inner- or outer-cellular stimuli. Atherosclerosis is characterized by a complex interaction of inflammation, lipid deposition, vascular smooth muscle cell proliferation, endothelial dysfunction, and extracellular matrix remodeling, which will result in the formation of an intimal plaque. Although the regulation and function of vascular smooth muscle cells are important in the progression of atherosclerosis, the roles of smooth muscle cells in regulating vascular inflammation are rarely focused upon, compared to those of endothelial cells or inflammatory cells. Therefore, in this review, we will discuss here how smooth muscle cells contribute or regulate the inflammatory reaction in the progression of atherosclerosis, especially in the context of the activation of various membrane receptors, and how they may regulate vascular inflammation.

Fig. 1.. Involvement of vSMCs in the inflammatory response of atherosclerosis. 1-5 briefly show LDL-induced inflammatory reactions, in which modified LDL particles are accumulated in the artery under various risk factors, resulting in the formation of form cells. This process is mediated by uptake of ox-LDL particles from the activation of scavenger receptors of macrophages, such as CD36, SRA1/2, LOX-1, and TLRs. In addition, SMCs can produce proinflammatory cytokines, through the activation of LOX-1, RAGE, TLR2, TLR4, AT1R, or NLRP3 by their specific agonists, and by their interaction with endothelial cells and macrophages.