Zhang Chenfei, Huang Xiaoling
Department of Gastroenterology, Xinjiang Medical University, Urumqi, China.
Department of Gastroenterology, People's Hospital of Xinjiang Uygur Autonomous Region, Urumqi, China.
Immunol Invest. 2025 Feb 17:1-19. doi: 10.1080/08820139.2025.2465644.
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.
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.
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.
TAK-242 exhibits therapeutic potential in the treatment of UC, and this research suggests further investigation and clinical trials to enhance patient outcomes.
溃疡性结肠炎（UC）是一种导致肠上皮溃疡和炎症的病症。UC的治疗取决于巨噬细胞从促炎（M1）表型向抗炎和组织修复（M2）表型的转变。据报道，组蛋白乳酰化的表观遗传改变会影响巨噬细胞的活性和表型。TAK - 242是一种TLR4抑制剂，可刺激组蛋白乳酰化以产生具有修复作用的M2型UC巨噬细胞。
本综述重点介绍了以下内容：引言部分的意义、组蛋白乳酰化概述、TAK - 242调节炎症反应的作用机制、TAK - 242与组蛋白乳酰化的关系、TAK - 242依赖性组蛋白乳酰化在巨噬细胞极化中的潜在作用、修复性巨噬细胞在溃疡性结肠炎中的作用以及组蛋白乳酰化对修复性巨噬细胞的调节。
溃疡性结肠炎的新型治疗方法包括使用TAK - 242增强组蛋白乳酰化，进而增强巨噬细胞功能并促进黏膜愈合。
TAK - 242在UC治疗中显示出治疗潜力，本研究建议进一步开展调查和临床试验以改善患者预后。
