TY - JOUR
T1 - The role of PCSK9 in intestinal lipoprotein metabolism
T2 - Synergism of statin and ezetimibe
AU - Fazio, Sergio
N1 - Funding Information:
Over the last 12 months Dr. Fazio has consulted for Merck, Genentech, Genzyme, ISIS, Kowa, Lupin, Sanofi, Roche, Basf, and Amarin. All consultations were scientific discussions about current and pipeline lipid agents. This work was funded by an unrestricted grant by MSD Italia Srl. The sponsor had no role in reviewing the literature, drafting or reviewing the paper, or in the decision to submit the manuscript for publication. All views expressed are solely those of the author. The author would like to thank Editamed Srl for editorial assistance in the preparation of the manuscript.
Publisher Copyright:
© 2015 Elsevier Ireland Ltd.
PY - 2015/2/1
Y1 - 2015/2/1
N2 - Proprotein convertase subtilisin/kexin type 9 (PCSK9) plays a major role in the regulation of lipoprotein metabolism, mostly through control of low-density lipoprotein receptor degradation. Depletion of cellular cholesterol causes a compensatory increase in plasma PCSK9 levels, which can diminish the cholesterol-lowering power of statins and may lead to the overproduction of intestinal lipoproteins, mainly thorough the up regulation of microsomal triglyceride transfer protein and the Niemann-Pick C1-like 1 protein, the target of ezetimibe. Thus, ezetimibe therapy may counter this unwanted effect of statins, providing an additional theoretical rationale for combining the effect of ezetimibe on intestinal cholesterol absorption and that of statins on cholesterol synthesis.
AB - Proprotein convertase subtilisin/kexin type 9 (PCSK9) plays a major role in the regulation of lipoprotein metabolism, mostly through control of low-density lipoprotein receptor degradation. Depletion of cellular cholesterol causes a compensatory increase in plasma PCSK9 levels, which can diminish the cholesterol-lowering power of statins and may lead to the overproduction of intestinal lipoproteins, mainly thorough the up regulation of microsomal triglyceride transfer protein and the Niemann-Pick C1-like 1 protein, the target of ezetimibe. Thus, ezetimibe therapy may counter this unwanted effect of statins, providing an additional theoretical rationale for combining the effect of ezetimibe on intestinal cholesterol absorption and that of statins on cholesterol synthesis.
KW - Ezetimibe
KW - LDL receptor
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U2 - 10.1016/S1567-5688(15)50006-8
DO - 10.1016/S1567-5688(15)50006-8
M3 - Article
C2 - 25659873
AN - SCOPUS:84924943883
VL - 17
SP - 23
EP - 26
JO - Atherosclerosis Supplements
JF - Atherosclerosis Supplements
SN - 1567-5688
ER -