ArticleExperimental and therapeutic medicine2021
Inhibition of heat shock protein 90 alleviates cholestatic liver injury by decreasing IL-1β and IL-18 expression.
Article in Experimental and therapeutic medicine, 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, 7 citations in OpenAlex.
- miR-223-3p predicts prognosis of hepatitis B virus-related acute-on-chronic liver failure and is involved in hepatocyte injury via HSP90B1.Hereditas · 2025Article
- Potential Hepatoprotective Effects ofAntioxidants (Basel, Switzerland) · 2023Article
- Review
- Interleukin-18 Binding Protein in Immune Regulation and Autoimmune Diseases.Biomedicines · 2022Review
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Authors and funding
8 authors at 4 institutions in 1 country.
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Abstract
Severe cholestatic liver injury diseases, such as obstructive jaundice and the subsequent acute obstructive cholangitis, are induced by biliary tract occlusion. Heat shock protein 90 (HSP90) inhibitors have been demonstrated to be protective for various organs. The potential of HSP90 inhibitors in the treatment of cholestatic liver injury, however, remains unclear. In the present study, rat models of bile duct ligation (BDL) were established, the HSP90 inhibitor 17-dimethylamino-ethylamino-17-demethoxygeldanamycin (17-DMAG) was administered, and its ability to ameliorate the cholestasis-induced liver injuries was evaluated. In the BDL rat models and clinical samples, increased HSP90 expression was observed to be associated with cholestatic liver injury. Furthermore, 17-DMAG alleviated cholestasis-induced liver injury in the rat models, as revealed by the assessment of pathological changes and liver function. In addition, 17-DMAG protected hepatocytes against cholestatic injury
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