ArticleInternational journal of medical sciences2021
REV-ERBα Agonist GSK4112 attenuates Fas-induced Acute Hepatic Damage in Mice.
Article in International journal of medical sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- The interplay between circadian rhythm components and apoptosis in health and disease.Human cell · 2026Review
- Rev‑erbα: The circadian guardian against NLRP3‑driven liver fibrosis.Molecular medicine reports · 2025Article
- Circadian Clock Disruption and Non-type 2 Asthma: A Hypothesis-Driven Perspective on Immune, Epithelial, and Steroid Response.Clinical reviews in allergy & immunology · 2025Review
- Targeting NR1D1 in organ injury: challenges and prospects.Military Medical Research · 2023Review
- Isolation, culture, and delivery considerations for the use of mesenchymal stem cells in potential therapies for acute liver failure.Frontiers in immunology · 2023Review
- Circadian Regulation of Gene Expression and Metabolism in the Liver.Seminars in liver disease · 2022Review
- Molecular regulations of circadian rhythm and implications for physiology and diseases.Signal transduction and targeted therapy · 2022Review
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fas-induced apoptosis is a central mechanism of hepatocyte damage during acute and chronic hepatic disorders. Increasing evidence suggests that circadian clock plays critical roles in the regulation of cell fates. In the present study, the potential significance of REV-ERBα, a core ingredient of circadian clock, in Fas-induced acute liver injury has been investigated. The anti-Fas antibody Jo2 was injected intraperitoneally in mice to induce acute liver injury and the REV-ERBα agonist GSK4112 was administered. The results indicated that treatment of GSK4112 decreased the level of plasma ALT and AST, attenuated the liver histological changes, and promoted the survival rate in Jo2-insulted mice. Treatment with GSK4112 also downregulated the activities of caspase-3 and caspase-8, suppressed hepatocyte apoptosis. In addition, treatment with GSK4112 decreased the level of Fas and enhanced the phosphorylation of Akt. In conclusion, treatment with GSK4112 alleviated Fas-induced apoptotic liver damage in mice, suggesting that REV-ERBα agonist might have potential value in pharmacological intervention of Fas-associated liver injury.
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