{"title":"Differentiation-inducing factor-1 ameliorates liver fibrosis through the reversion of activated hepatic stellate cells","authors":"Akira Ooka , Momoka Yamaguchi , Kensuke Suzuki , Shin-ya Saito , Yukiko K. Kaneko , Toshihide Kimura , Tomohisa Ishikawa","doi":"10.1016/j.bbadis.2025.167802","DOIUrl":null,"url":null,"abstract":"<div><div><ul><li><span>•</span><span><div>DIF-1 derived from <em>Dictyostelium discoideum</em> ameliorates liver fibrosis (LF) in mice.</div></span></li><li><span>•</span><span><div>When the LF mouse model was orally administered with DIF-1, decreased expression of <em>Acta2</em>, <em>Col1a1</em>, <em>Pdgfrb</em>, and <em>Timp1</em>, markers of activated hepatic stellate cells (HSCs) and genes related to LF, and increased expression of <em>Lrat</em>, a marker of quiescent HSCs, were observed in the liver tissue.</div></span></li><li><span>•</span><span><div>The treatment of primary cultured mouse activated HSCs with DIF-1 reverted the cell morphology to a quiescent HSC-like shape and significantly reduced the expression of α-smooth muscle actin, a marker of activated HSCs.</div></span></li></ul></div></div>","PeriodicalId":8821,"journal":{"name":"Biochimica et biophysica acta. Molecular basis of disease","volume":"1871 5","pages":"Article 167802"},"PeriodicalIF":4.2000,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biochimica et biophysica acta. Molecular basis of disease","FirstCategoryId":"99","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0925443925001474","RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/3/17 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
•
DIF-1 derived from Dictyostelium discoideum ameliorates liver fibrosis (LF) in mice.
•
When the LF mouse model was orally administered with DIF-1, decreased expression of Acta2, Col1a1, Pdgfrb, and Timp1, markers of activated hepatic stellate cells (HSCs) and genes related to LF, and increased expression of Lrat, a marker of quiescent HSCs, were observed in the liver tissue.
•
The treatment of primary cultured mouse activated HSCs with DIF-1 reverted the cell morphology to a quiescent HSC-like shape and significantly reduced the expression of α-smooth muscle actin, a marker of activated HSCs.
期刊介绍：
BBA Molecular Basis of Disease addresses the biochemistry and molecular genetics of disease processes and models of human disease. This journal covers aspects of aging, cancer, metabolic-, neurological-, and immunological-based disease. Manuscripts focused on using animal models to elucidate biochemical and mechanistic insight in each of these conditions, are particularly encouraged. Manuscripts should emphasize the underlying mechanisms of disease pathways and provide novel contributions to the understanding and/or treatment of these disorders. Highly descriptive and method development submissions may be declined without full review. The submission of uninvited reviews to BBA - Molecular Basis of Disease is strongly discouraged, and any such uninvited review should be accompanied by a coverletter outlining the compelling reasons why the review should be considered.
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