PCSK9 is a co-activator of platelet function beyond its role in cholesterol homeostasis, according to research presented at European Society of Cardiology (ESC) Congress on August 27, 2017, in Barcelona (August 26-30). The findings suggest that PCSK9 inhibitors, a new class of cholesterol-lowering treatments, may also reduce thrombosis by interfering with platelet activation. Proprotein convertase subtilisin/kexin 9 (PCSK9) is a main player in cholesterol homeostasis by inducing degradation of the low-density lipoprotein (LDL) cholesterol receptor. Emerging evidence indicates that plasma levels of PCSK9 predict recurrent cardiovascular events, for example myocardial infarction and angina, in patients with coronary artery disease, even in those with well controlled LDL cholesterol levels. "We hypothesized that the contribution of PCSK9 to cardiovascular events might be mediated by as yet unknown cholesterol-independent pathways," said last author Dr. Marina Camera, Associate Professor of Pharmacology, University of Milan, Italy. "It has been reported that increased plasma levels of PCSK9 are associated with platelet reactivity. However, no study has so far evaluated whether or not PCSK9 directly affects the function of platelets."
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