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Genetic and Pharmacologic Inactivation of ANGPTL3 and Cardiovascular Disease
Author(s) -
Frederick E. Dewey,
Viktoria Gusarova,
Richard L. Dunbar,
Colm O’Dushlaine,
Claudia Schurmann,
Omri Gottesman,
Shane McCarthy,
Cristopher V. Van Hout,
Shan Bruse,
Hayes M. Dansky,
Joseph B. Leader,
Michael F. Murray,
Marylyn D. Ritchie,
H. Lester Kirchner,
Lukas Habegger,
Alex Lopez,
John S. Penn,
An Sha Zhao,
Weiping Shao,
Neil Stahl,
Andrew Murphy,
Sara Hamon,
Aurelie Bouzelmat,
Rick Zhang,
Brad Shumel,
Robert Pordy,
Daniel A. Gipe,
Gary Herman,
Wayne HueyHerng Sheu,
ITe Lee,
KaeWoei Liang,
Xiuqing Guo,
Jerome I. Rotter,
YiiDer I. Chen,
William E. Kraus,
Svati H. Shah,
Scott M. Damrauer,
Aeron Small,
Daniel J. Rader,
Anders Berg Wulff,
Børge G. Nordestgaard,
Anne TybjærgHansen,
Anita M. van den Hoek,
P. Hans,
David H. Ledbetter,
David J. Carey,
John D. Overton,
Jeffrey G. Reid,
William J. Sasiela,
Poulabi Banerjee,
Alan R. Shuldiner,
Ingrid B. Borecki,
Tanya M. Teslovich,
George D. Yancopoulos,
Scott Mellis,
Jesper Gromada,
Aris Baras
Publication year - 2017
Publication title -
new england journal of medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 19.889
H-Index - 1030
eISSN - 1533-4406
pISSN - 0028-4793
DOI - 10.1056/nejmoa1612790
Subject(s) - medicine , cholesterol , disease , lipoprotein , endocrinology , atherosclerotic cardiovascular disease , genetic variants , gene , genetics , biology , genotype
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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