Jacquelyn J. Maher, MD
My laboratory studies basic mechanisms of hepatotoxicity, with a focus on clinically relevant diseases such as drug-induced liver injury and nonalcoholic steatohepatitis (NASH). One important goal is to identify hepatoprotective compounds that are therapeutic in the setting of acute liver failure or liver transplantation. In the setting of fatty liver, we are interested in the ability of specific fatty acids to cause liver cell death (“lipotoxicity”). We use cell culture and animal models to investigate how fat causes liver injury, and how the accumulation of toxic fatty acids in the liver might be avoided by dietary modifications such as lowering sugar consumption.
Nie B, Park HM, Kazantzis M, Lin M, Henkin A, Ng S, Song S, Chen Y, Tran H, Lai R, Her C, Maher JJ, Forman BM, Stahl A. Specific bile acids inhibit hepatic fatty acid uptake in mice. Hepatology. 2012 Oct;56(4):1300-10
Yin C, Evason KJ, Maher JJ, Stainier DY. The basic helix-loop-helix transcription factor, heart and neural crest derivatives expressed transcript 2, marks hepatic stellate cells in zebrafish: Analysis of stellate cell entry into the the developing liver. Hepatology. 2012 Nov;56(5):1958-70.
Maher JJ. New insights from rodent models of fatty liver disease. Antioxid Redox Signal. 2011 Jul 15;15(2):535-50.
Soon RK Jr, Yan JS, Grenert JP, Maher JJ. Stress signaling in the methionine-choline-deficient model of murine fatty liver disease. Gastroenterology. 2010 Nov;139(5):1730-9, 1739.e1.
- Program Director, UCSF Liver Center
- Hepatic Physiology and Metabolism
- Phone: (415) 206-4805
- Fax: (415) 641-0517
- San Francisco General Hospital
- 1001 Potrero Ave.
- Building 40, Room 4102
- San Francisco, CA 94110
Other UCSF Affiliations
- BMS Graduate Program
- Hellen Diller Family Comprehensive Cancer Center