ArticleCellular and molecular life sciences : CMLS2025
Fibulin-1 deficiency alleviates liver fibrosis by inhibiting hepatic stellate cell activation via the p38 MAPK pathway.
Article in Cellular and molecular life sciences : CMLS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Contribution of p38 MAPK in liver fibrosis: An overview of mechanisms, signaling pathways, and therapeutic targets (Review).International journal of molecular medicine · 2026Review
- Curcumin Targets Crispld2 to Suppress Hepatic Stellate Cell Activation via PI3K/AKT Pathway Inhibition in Hepatic Fibrosis.Liver international : official journal of the International Association for the Study of the Liver · 2026Article
- Shotgun Label-Free Proteomic Analysis for Identification of a Potential Diagnostic Biomarker for Pancreatic Cancer.Biomedicines · 2025Article
- Hydrogel Loaded with Aminoethyl Anisamide-Modified Exosomes Attenuates Hepatic Fibrosis by Targeting Activated Hepatic Stellate Cells.ACS nano · 2025Article
- Combined Analysis of Protein Induced by Prothrombin Induced by Vitamin K Absence (PIVKA) and Alpha-L-Fucosidase (AFU) with Alpha-Fetoprotein (AFP) May Improve the Diagnostic Efficacy for Liver Cirrhosis and Hepatocellular Carcinoma in Chronic Hepatitis B.International journal of general medicine · 2025Article
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11 authors.
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Abstract
Elastin stabilization has been correlated with the reversibility of fibrosis. Fibulin-1 can participate in elastin assembly, which promotes its stabilization. However, the role of Fibulin-1 in liver fibrosis remains unknown. Here, we performed a proteomics analysis to identify notable changes in Fibulin-1 expression during continuous fibrosis progression and regression. Fibulin-1 expression was dramatically increased in the plasma of patients with cirrhosis as well as in liver fibrosis models and hepatic stellate cells (HSCs) treated with TGF-β1, and significant accumulation of Fibulin-1 was observed in chronic hepatitis B (CHB)- and metabolic dysfunction-associated steatohepatitis (MASH)-related cirrhosis. Functional studies demonstrated that Fibulin-1 silencing inhibited HSC activation, while the opposite effects were observed for Fibulin-1 overexpression in vitro. Furthermore, transcriptomic analysis revealed that Fibulin-1 mediated p38 MAPK pathway activation, which was confirmed by the addition of a p38 MAPK inhibitor. More importantly, Fibulin-1 depletion in a CCl
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