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Gene Inactivation of Proprotein Convertase Subtilisin/Kexin Type 9 Reduces Atherosclerosis in Mice
Author(s) -
Maxime Denis,
Jadwiga Marcinkiewicz,
Ahmed Zaid,
Dany Gauthier,
Steve Poirier,
Claude Lazure,
Nabil G. Seidah,
Annik Prat
Publication year - 2012
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.111.057406
Subject(s) - kexin , pcsk9 , medicine , endocrinology , proprotein convertase , apolipoprotein b , ldl receptor , cholesterol , lipoprotein , familial hypercholesterolemia , genetically modified mouse , knockout mouse , subtilisin , receptor , apolipoprotein e , transgene , chemistry , biochemistry , enzyme , gene , disease
The proprotein convertase subtilisin/kexin type 9 (PCSK9) promotes independently of its enzymatic activity the degradation of the low-density lipoprotein (LDL) receptor. PCSK9 gain of function in humans leads to autosomal dominant hypercholesterolemia, whereas the absence of functional PCSK9 results in ≈7-fold lower levels of LDL cholesterol. This suggests that lowering PCSK9 may protect against atherosclerosis.

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