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CD36, a scavenger receptor implicated in atherosclerosis
CD36, a scavenger receptor implicated in atherosclerosis
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CD36, a scavenger receptor implicated in atherosclerosis
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CD36, a scavenger receptor implicated in atherosclerosis
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CD36, a scavenger receptor implicated in atherosclerosis
CD36, a scavenger receptor implicated in atherosclerosis
Journal Article

CD36, a scavenger receptor implicated in atherosclerosis

2014
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Overview
CD36 is a membrane glycoprotein that is present on various types of cells, including monocytes, macrophages, microvascular endothelial cells, adipocytes and platelets. Macrophage CD36 participates in atherosclerotic arterial lesion formation through its interaction with oxidized low-density lipoprotein (oxLDL), which triggers signaling cascades for inflammatory responses. CD36 functions in oxLDL uptake and foam cell formation, which is the initial critical stage of atherosclerosis. In addition, oxLDL via CD36 inhibits macrophage migration, which may be a macrophage-trapping mechanism in atherosclerotic lesions. The role of CD36 was examined in in vitro studies and in vivo experiments, which investigated various functions of CD36 in atherosclerosis and revealed that CD36 deficiency reduces atherosclerotic lesion formation. Platelet CD36 also promotes atherosclerotic inflammatory processes and is involved in thrombus formation after atherosclerotic plaque rupture. Because CD36 is an essential component of atherosclerosis, defining the function of CD36 and its corresponding signaling pathway may lead to a new treatment strategy for atherosclerosis. Atherosclerosis: Multiple roles of membrane protein CD36, a protein found on the surface of various immune cells and blood vessel cells, is a key component of atherosclerosis. Young Mi Park from the Ewha Womans University School of Medicine in Seoul, South Korea, reviews how the CD36 protein on macrophages binds to a form of ‘bad’ cholesterol called oxidized low-density lipoprotein. This binding triggers a series of reactions that leads to inflammation and the formation of foam cells, fat-laden immune cells involved in plaque-build up on the inner lining of blood vessels. CD36 on platelets also promotes inflammatory responses involved in blood clots after plaques rupture. Park argues that a better understanding of CD36 and its functions could lead to new treatments for atherosclerosis, a condition commonly associated with an increased risk of heart attack and stroke.