Abstract
In humans, smooth muscle cells (SMCs) are the main cell type in the artery medial layer, in pre-atherosclerotic diffuse thickening of the intima, and in all stages of atherosclerotic lesion development. SMCs secrete the proteoglycans responsible for the initial binding and retention of atherogenic lipoproteins in the artery intima, with this retention driving foam cell formation and subsequent stages of atherosclerosis. In this chapter we review current knowledge of the extracellular matrix generated by SMCs in medial and intimal arterial layers, their relationship to atherosclerotic lesion development and stabilization, how these findings correlate with mouse models of atherosclerosis, and potential therapies aimed at targeting the SMC matrix-lipoprotein interaction for atherosclerosis prevention.
Highlights
Smooth muscle is the involuntary nonskeletal form of muscle cells, present in hollow organs such as the stomach, intestine, bladder and uterus, the respiratory tract, and arteries and veins of the circulatory system
Smooth muscle cells (SMCs) take on alternate phenotypes and roles including increased proliferation, increased production of matrix proteoglycans, uptake of lipoproteins and foam cell formation, loss of SMC markers and expression of macrophage markers, and stabilization of arteries against plaque rupture
In this chapter we review extracellular matrix (ECM) production by SMCs and its critical role in mediating the lipoprotein retention that drives atherosclerotic lesion development
Summary
Smooth muscle is the involuntary nonskeletal form of muscle cells, present in hollow organs such as the stomach, intestine, bladder and uterus, the respiratory tract, and arteries and veins of the circulatory system. SMCs take on alternate phenotypes and roles including increased proliferation, increased production of matrix proteoglycans, uptake of lipoproteins and foam cell formation, loss of SMC markers and expression of macrophage markers, and stabilization of arteries against plaque rupture. As the major cell type of the pre-atherosclerotic and atherosclerotic intima, the phenotypic characteristics and products generated by synthetic phenotype SMCs are key determinants of atherosclerotic lesion development (Nakashima et al 2008). Some of these SMC products are components of the ECM (Wight 2018). Growth factors, cytokines, and chemokines that bind to ECM molecules
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