期刊
FREE RADICAL BIOLOGY AND MEDICINE
卷 136, 期 -, 页码 159-171出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2019.02.021
关键词
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资金
- NIH NHLBI [R01 HL111614, T32 HL134643, R01 HL111614-S]
- Medical College of Wisconsin Cardiovascular Center's A. O. Smith Fellowship Scholars Program
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.
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