ArticleActa pharmaceutica Sinica. B2024
Suppressing FXR promotes antiviral effects of bile acids
Article in Acta pharmaceutica Sinica. B, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Ursodeoxycholic acid inhibits pneumonia caused by PRCV through the activation of TLR4-IRF3 mediated type Ⅰ interferon pathway.Veterinary research · 2026Article
- From chemical composition to clinical application: the value of bile-based traditional Chinese medicines in the treatment of liver diseases.Frontiers in pharmacology · 2026Review
- Article
- Article
- STK39 inhibits antiviral immune response by inhibiting DCAF1-mediated PP2A degradation.Acta pharmaceutica Sinica. B · 2025Article
- Virus-host interaction mechanisms in interferon therapy for hepatitis B virus infection: recent advances.Frontiers in immunology · 2025Review
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Authors and funding
12 authors.
Funding
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Abstract
Bile acids (BAs) are natural metabolites in mammals and have the potential to function as drugs against viral infection. However, the limited understanding of chenodeoxycholic acid (CDCA) receptors and downstream signaling, along with its lower suppression efficiency in inhibiting virus infection limits its clinical application. In this study, we demonstrate that farnesoid X receptor (FXR), the receptor of CDCA, negatively regulates interferon signaling, thereby contributing to the reduced effectiveness of CDCA against virus replication. FXR deficiency or pharmacological inhibition enhances interferon signaling activation to suppress virus infection. Mechanistically, FXR impairs the DNA binding and transcriptional abilities of activated interferon regulatory factor 3 (IRF3) through interaction. Reduced IRF3 transcriptional activity by FXR-IRF3 interaction significantly undermines the expression of Interferon Beta 1 (IFNB1) and the antiviral response of cells, especially upon the CDCA treatment. In
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