J. Lipid Res.
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A more recent version of this article appeared on February 1, 2008

Papers In Press, published online ahead of print November 21, 2007
J. Lipid Res., doi:10.1194/jlr.M700437-JLR200
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Submitted on September 28, 2007
Revised on November 14, 2007
Accepted on November 20, 2007

Atorvastatin increases human serum levels of proprotein convertase subtilisin kexin type 9 (PCSK9)

Holly E. Careskey, R. Aleks Davis, William E. Alborn, Jason S. Troutt, Guoqing Cao, and Robert J. Konrad

Experimental Medicine, Eli Lilly and Company, Lilly Corporate Center, Indianapolis, IN 46285

Corresponding Author: konrad_robert{at}lilly.com

Proprotein convertase subtilisin kexin type 9 (PCSK9) has gained attention as a key regulator of serum LDL-cholesterol (LDL-C) levels. This novel protease causes the degradation of hepatic LDL receptors (LDLR). In humans, gain-of-function mutations in PCSK9 cause a form of familial hypercholesterolemia, while loss-of-function mutations result in significantly decreased LDL-C levels and cardiovascular risk. Previous studies have demonstrated that statins upregulate PCSK9 mRNA expression in cultured cells and animal models. In light of these observations, we studied the effect of atorvastatin on circulating PCSK9 protein levels in humans using a sandwich ELISA to quantitate serum PCSK9 levels in patients treated with atorvastatin or placebo for 16 weeks. We observed that atorvastatin (40 mg per day) significantly increased circulating PCSK9 levels 34% compared to baseline and placebo while lowering LDL-C levels by 42%. These results suggest that addition of a PCSK9 inhibitor to statin therapy may result in even further LDL-C lowering.


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