An AMPK–caspase-6 axis controls liver damage in nonalcoholic steatohepatitis
Abstract
The energy sensor adenosine monophosphate–activated protein kinase (AMPK) is implicated in liver damage in nonalcoholic steatohepatitis (NASH), a leading cause of liver-associated death in humans. Zhao et al. used mouse models of NASH and samples from human NASH patients to show that AMPK, the activity of which is lost in NASH, phosphorylates the enzyme procaspase-6. In normal liver cells, this modification limits the activation of caspase-6 and the consequent caspase activation cascade that leads to apoptosis. AMPK and caspase-6 may thus provide therapeutic targets for the treatment of NASH.
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- Feb 07, 2020
- Source ID
- 10.1126/science.aay0542
Entities
People
- Alan R. Saltiel
- Cynthia Chaggan
- Feng He
- Joseph L Witztum
- Kai In Wong
- Michael Karin
- Peng Zhao
- Rohit Loomba
- Seema Singh
- Xiaoli Sun
- Zhongji Liao
Organizations
- American Heart Association
- National Center for Advancing Translational Sciences
- National Heart, Lung, and Blood Institute
- National Institute of Diabetes and Digestive and Kidney Diseases
- National Institute of Environmental Health Sciences
- United States Department of Defense
- University of California, San Diego