Journal
LIVER INTERNATIONAL
Volume 38, Issue 8, Pages 1363-1374Publisher
WILEY
DOI: 10.1111/liv.13866
Keywords
acetaminophen; acetaminophen protein adducts; autophagy; liver injury; mitophagy
Categories
Funding
- NIH [R01 AA020518, R01 DK102142, U01 AA024733, P20GM103549, P30GM118247]
- CSC [201708040024]
Ask authors/readers for more resources
Acetaminophen (APAP) overdose is the most frequent cause of acute liver failure in the USA and many other countries. Although the metabolism and pathogenesis of APAP has been extensively investigated for decades, the mechanisms by which APAP induces liver injury are incompletely known, which hampers the development of effective therapeutic approaches to tackle this important clinical problem. Autophagy is a highly conserved intracellular degradation pathway, which aims at recycling cellular components and damaged organelles in response to adverse environmental conditions and stresses as a survival mechanism. There is accumulating evidence indicating that autophagy is activated in response to APAP overdose in specific liver zone areas, and pharmacological activation of autophagy protects against APAP-induced liver injury. Increasing evidence also suggests that hepatic autophagy is impaired in nonalcoholic fatty livers (NAFLD), and NAFLD patients are more susceptible to APAP-induced liver injury. Here, we summarized the current progress on the role and mechanisms of autophagy in protecting against APAP-induced liver injury.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available