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During ALI, the function of males absent on the first (MOF) has not yet been elucidated. In this study, we unveiled the expression pattern of MOF during carbon tetrachloride (CCl<jats:sub>4<\/jats:sub>)\u2010induced ALI and role of MOF in the regulation of liver regeneration. In the process of ALI, MOF is significantly overexpressed in the liver injury area. Knockdown of <jats:italic>Mof<\/jats:italic> attenuated CCl<jats:sub>4<\/jats:sub>\u2010induced ALI, and promoted liver cell proliferation, hepatic stellate cell activation and aggregation to the injured area, and liver fibrosis. Simultaneously, overexpression of <jats:italic>Mof<\/jats:italic> aggravated liver dysfunction caused by ALI. By directly binding to the promoter, MOF suppressed the transcriptional activation of <jats:italic>Igf1<\/jats:italic>. Knockdown of <jats:italic>Mof<\/jats:italic> promotes the expression of <jats:italic>Igf1<\/jats:italic> and activates the Insulin\u2010like growth factor 1 signaling pathway in the liver. Through this pathway, Knockdown of <jats:italic>Mof<\/jats:italic> reduces CCl<jats:sub>4<\/jats:sub>\u2010induced ALI and promotes liver regeneration. Our results provide the first demonstration for MOF contributing to ALI. Further understanding of the role of MOF in ALI may lead to new therapeutic strategies for ALI.<\/jats:p>","DOI":"10.1002\/jcp.30332","type":"journal-article","created":{"date-parts":[[2021,2,26]],"date-time":"2021-02-26T08:31:03Z","timestamp":1614328263000},"page":"6559-6570","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["Lack of <i>Mof<\/i> reduces acute liver injury by enhancing transcriptional activation of <i>Igf1<\/i>"],"prefix":"10.1002","volume":"236","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0650-2170","authenticated-orcid":false,"given":"Meng","family":"Wang","sequence":"first","affiliation":[{"name":"Shandong Provincial Key Laboratory of Animal Cell and Developmental Biology, School of Life Sciences, Advanced Medical Research Institute Shandong University  Qingdao Shandong China"},{"name":"Department of Cell and Neurobiology, School of Basic Medical Sciences Shandong University  Jinan Shandong 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