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Proprotein Convertase Subtilisin Kexin Type 9 Promotes Intestinal Overproduction of Triglyceride-Rich Apolipoprotein B Lipoproteins Through Both Low-Density Lipoprotein Receptor–Dependent and –Independent Mechanisms
Author(s) -
Shirya Rashid,
Hagai Tavori,
Patrick Brown,
MacRae F. Linton,
Jane He,
Ilaria Giunzioni,
Sergio Fazio
Publication year - 2014
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/circulationaha.113.006720
Subject(s) - kexin , proprotein convertase , pcsk9 , subtilisin , medicine , apolipoprotein b , overproduction , triglyceride , lipoprotein , endocrinology , apolipoprotein c2 , ldl receptor , very low density lipoprotein , biochemistry , cholesterol , biology , gene , enzyme
Proprotein convertase subtilisin kexin type 9 (PCSK9) promotes the degradation of the low-density lipoprotein (LDL) receptor (LDLR), and its deficiency in humans results in low plasma LDL cholesterol and protection against coronary heart disease. Recent evidence indicates that PCSK9 also modulates the metabolism of triglyceride-rich apolipoprotein B (apoB) lipoproteins, another important coronary heart disease risk factor. Here, we studied the effects of physiological levels of PCSK9 on intestinal triglyceride-rich apoB lipoprotein production and elucidated for the first time the cellular and molecular mechanisms involved.

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