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Bile acids and coronavirus disease 2019

Huang et al., Acta Pharmaceutica Sinica B, doi:10.1016/j.apsb.2024.02.011
Feb 2024  
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Review of the relationship between bile acids and COVID-19. Authors discuss emerging basic and clinical evidence linking bile acids to COVID-19 infection and potential mechanisms. Functionally, studies indicate that certain bile acids like ursodeoxycholic acid may protect against SARS-CoV-2 infection by modulating ACE2 expression or activity. Mechanistically, bile acids influence pathways involving immunomodulation, inflammation, and metabolism that likely contribute to COVID-19 pathogenesis. Bile acid receptors FXR and TGR5 in particular participate in regulating ACE2 as well as immune responses, making them potential therapeutic targets.
See Fiorucci et al. for another review covering ursodeoxycholic acid for COVID-19.
Huang et al., 13 Feb 2024, peer-reviewed, 3 authors. Contact:
This PaperUDCAAll
Bile acids and coronavirus disease 2019
Xiaoru Huang, Xuening Liu, Zijian Li
Acta Pharmaceutica Sinica B, doi:10.1016/j.apsb.2024.02.011
The coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has been significantly alleviated. However, long-term health effects and prevention strategy remain unresolved. Thus, it is essential to explore the pathophysiological mechanisms and intervention for SARS-CoV-2 infection. Emerging research indicates a link between COVID-19 and bile acids, traditionally known for facilitating dietary fat absorption. The bile acid ursodeoxycholic acid potentially protects against SARS-CoV-2 infection by inhibiting the farnesoid X receptor, a bile acid nuclear receptor. The activation of G-protein-coupled bile acid receptor, another membrane receptor for bile acids, has also been found to regulate the expression of angiotensin-converting enzyme 2, the receptor through which the virus enters human cells. Here, we review the latest basic and clinical evidence linking bile acids to SARS-CoV-2, and reveal their complicated pathophysiological mechanisms.
Author contributions Xiaoru Huang and Xuening Liu contributed equally to this work. Xiaoru Huang and Xuening Liu drafted the manuscript; Xuening Liu prepared figures; Xiaoru Huang, Xuening Liu, and Zijian edited and revised the manuscript. Conflicts of interest The authors declare no conflicts of interest.
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