{"title":"Role of TAK-242-Induced Histone Lactylation in Modulating Repair Macrophage Transformation in Ulcerative Colitis.","authors":"Chenfei Zhang, Xiaoling Huang","doi":"10.1080/08820139.2025.2465644","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Ulcerative Colitis (UC) is a condition that causes ulceration and inflammation of the intestinal epithelium. UC treatment depends on macrophages' phenotypic switch from pro-inflammatory (M1) to anti-inflammatory and tissue-repairing (M2). It has been reported that the epigenetic alteration of histone lactylation affects macrophage activity and phenotype. TAK-242, a TLR4 inhibitor, stimulates histone lactylation to generate reparative M2 UC macrophages.</p><p><strong>Methods: </strong>This review highlighted the significance in terms of introduction, an overview of histone lactylation, the mechanism of action of TAK-242 in regulating inflammatory responses, the relationship between TAK-242 to histone lactylation, the potential role of TAK-242-dependent histone lactylation in macrophage polarization, the role of repair macrophages in ulcerative colitis and regulation of repair macrophages by histone lactylation.</p><p><strong>Results: </strong>Novel treatments for ulcerative colitis involve the use of TAK-242 to enhance histone lactylation, which in turn boosts macrophage function and promotes mucosal healing.</p><p><strong>Conclusion: </strong>TAK-242 exhibits therapeutic potential in the treatment of UC, and this research suggests further investigation and clinical trials to enhance patient outcomes.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-19"},"PeriodicalIF":2.9000,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Immunological Investigations","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/08820139.2025.2465644","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Background: Ulcerative Colitis (UC) is a condition that causes ulceration and inflammation of the intestinal epithelium. UC treatment depends on macrophages' phenotypic switch from pro-inflammatory (M1) to anti-inflammatory and tissue-repairing (M2). It has been reported that the epigenetic alteration of histone lactylation affects macrophage activity and phenotype. TAK-242, a TLR4 inhibitor, stimulates histone lactylation to generate reparative M2 UC macrophages.
Methods: This review highlighted the significance in terms of introduction, an overview of histone lactylation, the mechanism of action of TAK-242 in regulating inflammatory responses, the relationship between TAK-242 to histone lactylation, the potential role of TAK-242-dependent histone lactylation in macrophage polarization, the role of repair macrophages in ulcerative colitis and regulation of repair macrophages by histone lactylation.
Results: Novel treatments for ulcerative colitis involve the use of TAK-242 to enhance histone lactylation, which in turn boosts macrophage function and promotes mucosal healing.
Conclusion: TAK-242 exhibits therapeutic potential in the treatment of UC, and this research suggests further investigation and clinical trials to enhance patient outcomes.
期刊介绍：
Disseminating immunological developments on a worldwide basis, Immunological Investigations encompasses all facets of fundamental and applied immunology, including immunohematology and the study of allergies. This journal provides information presented in the form of original research articles and book reviews, giving a truly in-depth examination of the latest advances in molecular and cellular immunology.
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