ArticleDigestive diseases and sciences2026
S100A6 Regulated by PATZ1 Promotes Liver Fibrosis by Activating Hepatic Stellate Cells.
Article in Digestive diseases and sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
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- Moving Forward: Does Early Mobilization Benefit Patients with Acute Pancreatitis?Digestive diseases and sciences · 2026Article
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9 authors.
Funding
Abstract
backgroundThe transition of hepatic stellate cells (HSCs) from a quiescent state to active myofibroblasts plays a pivotal role in the progression of hepatic fibrosis. While S100A6, a member of the S100 protein family, and PATZ1, a transcriptional regulator, are speculated to play crucial roles in the fibrotic process, their specific functions and interactions in the liver fibrosis remain incompletely understood.
methodsC57BL/6 mice were administrated with CCl
resultsAnalysis of data from the GEO database revealed that PATZ1 expression was significantly decreased in liver cirrhosis patients, negatively correlated with the severity of fibrosis. Overexpression of PATZ1 could inhibit HSCs activation and alleviate liver fibrosis in vivo, as evidenced by downregulated fibrotic markers and decreased fibrotic areas in mice with hepatic fibrosis. Conversely, S100A6 expression was progressively upregulated during liver fibrosis progression, particularly in activated HSCs. Knockdown of S100A6 inhibited HSCs activation and alleviated liver fibrosis both in vitro and in vivo. Mechanistically, RNA-seq analysis suggested PATZ1 negatively regulated S100A6 expression in the activation process of HSCs, and EMSA further confirmed that PATZ1 could binding to the promoter of S100A6 gene.
conclusionS100A6 acted as a downstream target of PATZ1 during HSC activation, and PATZ1 could inhibit HSCs activation through suppression the expression of S100A6. PATZ1/S100A6 offered a potential therapeutic target for the therapy of liver fibrosis.
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