ArticleCellular and molecular life sciences : CMLS2024
GPR116 alleviates acetaminophen-induced liver injury in mice by inhibiting endoplasmic reticulum stress.
Article in Cellular and molecular life sciences : CMLS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The trial behind it
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Who cites it
3 citing papers in PubMed.
- Malic Enzyme 1 Limits Acetaminophen-Induced Liver Injury by Sustaining Redox and Bioenergetic Homeostasis.Metabolites · 2026Article
- DNAJB4/HLJ1 protects against acetaminophen-induced liver injury by attenuating ER stress via HSP70.Cell biology and toxicology · 2026Article
- Adhesion G protein-coupled receptors.Pharmacological reviews · 2026Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
backgroundAcetaminophen (APAP) overdose is a significant contributor to drug-induced liver injury worldwide. G-protein-coupled receptor 116 (GPR116) is an important homeostatic maintenance molecule in the body, but little is known about its role in APAP-induced liver injury (AILI).
methodsGPR116 expression was determined in both human and mouse AILI models. Hepatic function and damage response were analyzed in hepatocyte-specific GPR116 deletion (GPR116
resultsIntrahepatic GPR116 was upregulated in human and mice with AILI. GPR116
conclusionsUpregulation of GPR116 on hepatocytes inhibits ER stress by binding to β-arrestin1, protecting mice from APAP-induced hepatotoxicity. GPR116 may serve as a promising therapeutic target for AILI.
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