Journal
DRUG NEWS & PERSPECTIVES
Volume 21, Issue 6, Pages 323-330Publisher
PROUS SCIENCE, SAU-THOMSON REUTERS
DOI: 10.1358/dnp.2008.21.6.1246795
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Funding
- American Heart Association Florida [0555334B]
- University of South Florida, College of Medicine and Department of Molecular Medicine
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Proprotein convertase subtilisin/kexin type 9 (PCSK9) plays a critical role controlling the levels of low-density lipoprotein (LDL) particles that circulate in the bloodstream. Several gain-of-function and loss-of-function mutations in the PCSK9 gene, which occur naturally, have been identified and linked to hypercholesterolemia and hypocholesterolemia, respectively. Studies have demonstrated that PCSK9 acts mainly by enhancing degradation of the LDL receptor (LDLR) protein in the liver. Inactivation of PCSK9 in mice reduces plasma cholesterol levels primarily by increasing hepatic expression of LDLR protein and thereby accelerating clearance of circulating LDL cholesterol. Since the loss of a functional PCSK9 in human is not associated with apparent deleterious effects, this protease is becoming an attractive target for lowering plasma LDL cholesterol levels either alone or in combination with statins. (C) 2008 Prous Science, S.A.U. or its licensors. All rights reserved.
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