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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)\u2010induced liver fibrosis and Transforming Growth Factor\u2010Beta 1 (TGF\u2010\u03b21)\u2010activated HSCs. Knockdown of MFAP2 inhibited HSC proliferation and partially attenuated TGF\u2010\u03b2\u2010stimulated fibrogenesis markers. Bioinformatics analysis revealed that Fibrillin\u20101 (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\u2010induced mouse model. In conclusion, our results suggest that MFAP2 is a potential target for the clinical treatment of liver fibrosis.<\/jats:p>","DOI":"10.1111\/jcmm.17884","type":"journal-article","created":{"date-parts":[[2023,8,28]],"date-time":"2023-08-28T05:15:10Z","timestamp":1693199710000},"page":"3235-3246","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["<scp>MFAP2<\/scp> promotes <scp>HSCs<\/scp> activation through <scp>FBN1<\/scp>\/<scp>TGF<\/scp>\u2010\u03b2\/Smad3 pathway"],"prefix":"10.1111","volume":"27","author":[{"given":"Yonghong","family":"Sun","sequence":"first","affiliation":[{"name":"Department of Gastroenterology The First Hospital of Lanzhou University  Lanzhou China"},{"name":"Department of Pediatrics Gansu Province People's Hospital  Lanzhou People's Republic of 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