ArticleHepatology international2026
USP13 promotes hepatic stellate cells activation and aggravates liver fibrosis through deubiquitinating SMAD3.
Article in Hepatology international, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Integrating Network Pharmacology and Experimental Validation to Elucidate the Role of Huaier in Attenuating Liver Fibrosis via the AKT Signalling Pathway.Clinical and experimental medicine · 2026Article
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14 authors.
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Abstract
BACKGROUND/
aimsActivation of hepatic stellate cells (HSCs) is key to the development of liver fibrosis. Recent studies have highlighted the role of deubiquitinating enzymes (DUBs) in regulating protein stability and function, closely related to liver fibrosis. In this study, we screened out a key DUB, ubiquitin-specific peptidase 13 (USP13), in HSCs activation and explored its role and underlying mechanism.
methodsGene Expression Omnibus (GEO) public database were used to demonstrate the correlation of USP13 with HSC activation. Mice with adeno-associated virus (AAV)-mediated HSC-specific USP13 deficiency are proceeded to carbon tetrachloride (CCl
resultsWe first found that USP13 expression was upregulated in activated HSCs and in both CCl
conclusionsThis study illustrates an HSC-specific USP13-SMAD3 axis in regulating liver fibrosis and presents USP13 as a potential target for the treatment of liver fibrosis.
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