Human PCSK9 promotes hepatic lipogenesis and atherosclerosis development via apoE- and LDLR-mediated mechanisms

Conclusions PCSK9 increases hepatic lipid and lipoprotein production via apoE- and LDLR-dependent mechanisms. However, hPCSK9 also accumulate in the artery wall and directly affects atherosclerosis lesion size and composition independently of such plasma lipid and lipoprotein changes. These effects of hPCSK9 are dependent on LDLR but are independent of apoE.

http://cardiovascres.oxfordjournals.org/cgi/content/short/110/2/268?rss=1

Source: Cardiovascular Research - April 18, 2016 Category: Cardiology Authors: Tavori, H., Giunzioni, I., Predazzi, I. M., Plubell, D., Shivinsky, A., Miles, J., Devay, R. M., Liang, H., Rashid, S., Linton, M. F., Fazio, S. Tags: Vascular Biology Source Type: research