ArticleMolecular medicine reports2025
Rev‑erbα: The circadian guardian against NLRP3‑driven liver fibrosis.
Article in Molecular medicine reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed.
- The circadian clock controls hepatic stellate cell activation via a BMAL1/CK1ε/REV-ERBα/transgelin signaling pathway.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Multi-Omics Landscape of Circadian Clock Dysregulation Across the Chronic Liver Disease Spectrum.International journal of molecular sciences · 2026Review
- Circadian clock regulation in lung health and disease: molecular mechanisms and therapeutic opportunities.EXCLI journal · 2026Review
- Time to Reset: The Interplay Between Circadian Rhythms and Redox Homeostasis in Skeletal Muscle Ageing and Systemic Health.Antioxidants (Basel, Switzerland) · 2025Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Liver fibrosis is a pivotal pathological process in the progression of various chronic liver diseases toward cirrhosis, primarily driven by the activation of hepatic stellate cells. Recent studies have implicated dysregulation of circadian clock genes in the pathogenesis of hepatic disorders. The present investigation focused on the role of the circadian regulator nuclear receptor subfamily 1 group D member 1 (Rev‑erbα) in liver fibrosis and its mechanistic interplay with the NLR family domain containing protein 3 (NLRP3) inflammasome. A mouse model of liver fibrosis was established via carbon tetrachloride (CCl4) administration. The expression of Rev‑erbα was modulated pharmacologically using the agonist GSK4112 and the antagonist SR8278 to assess its impact on fibrogenesis. In parallel, lentiviral vectors were employed in
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