ArticleCell & bioscience2021
Rev-erbα exacerbates hepatic steatosis in alcoholic liver diseases through regulating autophagy.
Article in Cell & bioscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 13 citations in OpenAlex.
- Berberine alleviates alcoholic liver diseaseactivating intestinal nuclear receptor subfamily 1 group D member 1.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2026Article
- Rev‑erbα: The circadian guardian against NLRP3‑driven liver fibrosis.Molecular medicine reports · 2025Article
- Research progress on the mutual regulatory mechanism of circadian clock genes and autophagy.Frontiers in cell and developmental biology · 2025Review
- Article
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9 authors at 1 institution in 1 country.
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Abstract
BACKGROUND AND
aimsAlcoholic fatty liver (AFL) is a liver disease caused by long-term excessive drinking and is characterized by hepatic steatosis. Understanding the regulatory mechanism of steatosis is essential for the treatment of AFL. Rev-erbα is a member of the Rev-erbs family of nuclear receptors, playing an important role in regulating lipid metabolism. However, its functional role in AFL and its underlying mechanism remains unclear.
resultsRev-erbα was upregulated in the liver of EtOH-fed mice and EtOH-treated L-02 cells. Further, Rev-erbα activation exacerbates steatosis in L-02 cells. Inhibition/downexpression of Rev-erbα improved steatosis. Mechanistically, autophagy activity was inhibited in vivo and vitro. Interestingly, inhibition/downexpression of Rev-erbα enhanced autophagy. Furthermore, silencing of Rev-erbα up-regulated the nuclear expression of Bmal1. Autophagy activity was inhibited and steatosis was deteriorated after EtOH-treated L-02 cells were cotransfected with Rev-erbα shRNA and Bmal1 siRNA.
conclusionsRev-erbα induces liver steatosis, which promotes the progression of AFL. Our study reveals a novel steatosis regulatory mechanism in AFL and suggest that Rev-erbα might be a potential therapeutic target for AFL.
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