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Many patients with atherosclerosis have oxidative stress and a prothrombotic state, particularly in the presence of dyslipidemia. A Cleveland research team has found one molecular explanation, with therapeutic implications.
The team reports that oxidized LDL, and particularly a component of oxidized LDL called oxPCCD36, binds to and activates the CD36 receptor on platelets. In addition, oxPCCD36 impairs endothelial function and increases foam cell concentration within plaques. In mice, this process was particularly likely to occur when they were fed a high-fat diet. When the investigators extended the study to humans, they found a similar connection between oxPCCD36, platelet CD36, and a prothrombotic state. They speculate that, because HDL …