CD36 signaling in vascular redox stress. Free Radic Biol Med 2019 May 20;136:159-171
Date
03/03/2019Pubmed ID
30825500Pubmed Central ID
PMC6488418DOI
10.1016/j.freeradbiomed.2019.02.021Scopus ID
2-s2.0-85062659543 (requires institutional sign-in at Scopus site) 41 CitationsAbstract
Scavenger receptor CD36 is a multifunctional membrane protein that promotes thrombosis in conditions of oxidative stress such as metabolic disorders including dyslipidemia, diabetes mellitus, and chronic inflammation. In these conditions, specific reactive oxidant species are generated that are context and cell dependent. In the vasculature, CD36 signaling in smooth muscle cells and endothelial cells promotes generation of reactive oxygen species, genetic downregulation of antioxidant genes, and impaired smooth muscle and endothelial function. In hematopoietic cells, CD36 signaling enhances platelet dysfunction thus decreasing the threshold for platelet activation and accelerating arterial thrombosis, whereas in macrophages, CD36 promotes lipid-laden foam cell formation and atherosclerosis. These clinically significant processes are mediated through complex redox regulated signaling mechanisms that include Src-family kinases, MAP kinases and other downstream effectors. We provide an overview of CD36 signaling in vascular redox stress highlighting the role in oxidant generation in vascular and hematopoietic cells, but with special emphasis on platelets and dyslipidemia.
Author List
Yang M, Silverstein RLAuthor
Roy L. Silverstein MD Professor in the Medicine department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsBlood Platelets
CD36 Antigens
Dyslipidemias
Endothelial Cells
Humans
Oxidation-Reduction
Oxidative Stress
Platelet Activation
Signal Transduction
