ArticleJournal of cellular and molecular medicine2023
MFAP2 promotes HSCs activation through FBN1/TGF-β/Smad3 pathway.
Article in Journal of cellular and molecular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 9 citations in OpenAlex.
- <p>Beyond hepatic stellate cell heterogeneity: Resolving fibrosis, restoring regeneration (Review)</p>.International journal of molecular medicine · 2026Review
- [Cajanonic acid A derivative XJ-60 improves liver fibrosis in mice with non-alcoholic fatty liver disease by inhibiting the SP1/TGF-β/Smad3 signaling axis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- FOXA1-mediated transcription of MFAP2 facilitates cell growth, metastasis and cisplatin resistance in uterine corpus endometrial carcinoma.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Overexpression miR-125a-5p inhibits HSCs activation and alleviates liver fibrosis through TGF-β/Smad2/3 signaling pathway and autophagy.Cell death discovery · 2025Article
- Development of machine learning models for diagnostic biomarker identification and immune cell infiltration analysis in PCOS.Journal of ovarian research · 2025Article
- Hepatic stellate cell-derived microfibrillar-associated protein 2 prevents liver fibrosis by regulating extracellular matrix and inflammation.Theranostics · 2025Article
- Construction of a HSC activation-related lncRNA-miRNA-mRNA ceRNA regulatory network reveals potential molecules involved in liver fibrosis.Frontiers in genetics · 2025Article
- Curcumin Promotes Diabetic Foot Ulcer Wound Healing by Inhibiting miR-152-3p and Activating the FBN1/TGF-β Pathway.Molecular biotechnology · 2024Article
- MFAP2 promotes HSCs activation through FBN1/TGF-β/Smad3 pathway.Journal of cellular and molecular medicine · 2023Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Liver fibrosis is a chronic inflammatory process characterized by the accumulation of extracellular matrix (ECM), which contributes to cirrhosis and hepatocellular carcinoma. Increasing evidence suggests that the activation of hepatic stellate cells (HSCs) under an inflammatory state leads to the secretion of collagens, which can cause cirrhosis. In this study, we analysed data from the Gene Expression Omnibus (GEO) databases to identify differentially expressed genes (DEGs) between quiescent and fibrotic HSCs. We found that Microfibril Associated Protein 2 (MFAP2) was elevated in carbon tetrachloride (CCl4)-induced liver fibrosis and Transforming Growth Factor-Beta 1 (TGF-β1)-activated HSCs. Knockdown of MFAP2 inhibited HSC proliferation and partially attenuated TGF-β-stimulated fibrogenesis markers. Bioinformatics analysis revealed that Fibrillin-1 (FBN1) was correlated with MFAP2, and the expression of FBN1 was significantly upregulated after MFAP2 overexpression. Silencing MFAP2 partially attenuated the activation of HSCs by inhibiting HSC proliferation and decreasing collagen deposits. In vitro results showed that the inhibition of MFAP2 alleviated hepatic fibrosis by inhibiting the activation and inducing the apoptosis of active HSCs in a CCl4-induced mouse model. In conclusion, our results suggest that MFAP2 is a potential target for the clinical treatment of liver fibrosis.
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