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Genetic and Pharmacologic Inactivation of ANGPTL3 and Cardiovascular Disease
Authors
Frederick Dewey,Viktoria Gusarova
Richard Dunbar,Colm O’Dushlaine,Claudia Schurmann,Omri Gottesman,Shane McCarthy,Cristopher Hout,Shannon Bruse,Hayes Dansky,Joseph Leader,Michael Murray,Marylyn Ritchie,H. Kirchner,Lukas Habegger,Alex Lopez,John Penn,An Zhao,Weiping Shao,Neil Stahl,Andrew Murphy,Sara Hamon,Aurelie Bouzelmat,Rick Zhang,Brad Shumel,Robert Pordy,Daniel Gipe,Gary Herman,Wayne Sheu,I‐Te Lee,Kae‐Woei Liang,Xiuqing Guo,Jerome Rotter,Yii‐Der Chen,William Kraus,Svati Shah,Scott Damrauer,Aeron Small,Daniel Rader,Anders Wulff,Børge Nordestgaard,Anne Tybjærg‐Hansen,Anita Hoek,P. Hans,David Ledbetter,David Carey,John Overton,Jeffrey Reid,William Sasiela,Poulabi Banerjee,Alan Shuldiner,Ingrid Borecki,Jan Staessen,George Yancopoulos,Scott Mellis,Jesper Gromada,Aris Baras,Alanna Morrison
+56 authors
,Colm Ó'DúshláinePublished
May 24, 2017
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Abstract
Loss-of-function variants in the angiopoietin-like 3 gene (ANGPTL3) have been associated with decreased plasma levels of triglycerides, low-density lipoprotein (LDL) cholesterol, and high-density lipoprotein (HDL) cholesterol. It is not known whether such variants or therapeutic antagonism of ANGPTL3 are associated with a reduced risk of atherosclerotic cardiovascular disease.
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