A
Ariel E. Feldstein
Researcher at University of California, San Diego
Publications - 264
Citations - 29641
Ariel E. Feldstein is an academic researcher from University of California, San Diego. The author has contributed to research in topics: Nonalcoholic fatty liver disease & Fatty liver. The author has an hindex of 69, co-authored 245 publications receiving 24604 citations. Previous affiliations of Ariel E. Feldstein include Cleveland Clinic Lerner Research Institute & Cleveland Clinic.
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Journal ArticleDOI
Gut flora metabolism of phosphatidylcholine promotes cardiovascular disease
Zeneng Wang,Elizabeth Klipfell,Brian J. Bennett,Robert A. Koeth,Bruce S. Levison,Brandon DuGar,Ariel E. Feldstein,Earl B. Britt,Xiaoming Fu,Yoon-Mi Chung,Yuping Wu,Phil Schauer,Jonathan D. Smith,Hooman Allayee,W.H. Wilson Tang,Joseph A. DiDonato,Aldons J. Lusis,Stanley L. Hazen +17 more
TL;DR: Discovery of a relationship between gut-flora-dependent metabolism of dietary phosphatidylcholine and CVD pathogenesis provides opportunities for the development of new diagnostic tests and therapeutic approaches for atherosclerotic heart disease.
Journal ArticleDOI
The Natural History of Nonalcoholic Fatty Liver Disease: A Population-Based Cohort Study
Leon A. Adams,James F. Lymp,Jenny St. Sauver,Schuyler O. Sanderson,Keith D. Lindor,Ariel E. Feldstein,Paul Angulo +6 more
TL;DR: Mortality among community-diagnosed NAFLD patients is higher than the general population and is associated with older age, impaired fasting glucose, and cirrhosis, although the absolute risk is low.
Journal ArticleDOI
Hepatocyte apoptosis and fas expression are prominent features of human nonalcoholic steatohepatitis.
Ariel E. Feldstein,Ali Canbay,Paul Angulo,Makiko Taniai,Lawrence J. Burgart,Keith D. Lindor,Gregory J. Gores +6 more
TL;DR: Hepatocyte apoptosis is significantly increased in patients with NASH and correlates with disease severity, suggesting that antiapoptotic therapy may be useful in this syndrome.
Journal ArticleDOI
Free fatty acids promote hepatic lipotoxicity by stimulating TNF‐α expression via a lysosomal pathway
Ariel E. Feldstein,Nathan W. Werneburg,Ali Canbay,Maria Eugenia Guicciardi,Steven F. Bronk,Robert Rydzewski,Laurence J. Burgart,Gregory J. Gores +7 more
TL;DR: In a dietary murine model of NAFLD, either genetic or pharmacological inactivation of ctsb protected against development of hepatic steatosis, liver injury, and insulin resistance with its associated “dysmetabolic syndrome.”
Journal ArticleDOI
NLRP3 inflammasome activation results in hepatocyte pyroptosis, liver inflammation, and fibrosis in mice.
Alexander Wree,Akiko Eguchi,Matthew D. McGeough,Carla A. Peña,Casey D. Johnson,Ali Canbay,Hal M. Hoffman,Ariel E. Feldstein +7 more
TL;DR: It is demonstrated that global and, to a lesser extent, myeloid‐specific NLRP3 inflammasome activation results in severe liver inflammation and fibrosis while identifying hepatocyte pyroptotic cell death as a novel mechanism ofNLRP3‐mediated liver damage.