Emerging role of m6A modification in fibrotic diseases and its potential therapeutic effect

被引:4
|
作者
Ye, Wufei [1 ]
Lv, Xiongwen [2 ]
Gao, Songsen [3 ]
Li, Yueran [1 ]
Luan, Jiajie [1 ]
Wang, Sheng [1 ,4 ]
机构
[1] Yijishan Hosp, Affiliated Hosp 1, Dept Pharm, Wannan Med Coll, Wuhu, Anhui, Peoples R China
[2] Anhui Med Univ, Sch Pharm, Key Lab Antiinflammatory & Immune Med,Minist Educ, Anhui Prov Key Lab Major Autoimmune Dis,Inst Liver, Hefei, Anhui, Peoples R China
[3] Anhui Med Univ, Dept Orthoped Spinal Surg, Affiliated Hosp 1, Hefei, Anhui, Peoples R China
[4] Yijishan Hosp, Wannan Med Coll, Dept Pharm, Affiliated Hosp 1, 2 Zheshan West Rd, Wuhu 241001, Anhui, Peoples R China
基金
中国国家自然科学基金;
关键词
Fibrotic diseases; m6A modification; METTL3; RNA metabolism; Therapeutic targets; STELLATE CELL ACTIVATION; ATTENUATES LIVER FIBROSIS; RNA-METHYLATION; TGF-BETA; RETINAL FIBROSIS; CARDIAC FIBROSIS; GENE-EXPRESSION; NUCLEAR-RNA; M(6)A; TRANSLATION;
D O I
10.1016/j.bcp.2023.115873
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Fibrosis can occur in a variety of organs such as the heart, lung, liver and kidney, and its pathological changes are mainly manifested by an increase in fibrous connective tissue and a decrease in parenchymal cells in organ tissues, and continuous progression can lead to structural damage and organ hypofunction, or even failure, seriously threatening human health and life. N6-methyladenosine (m6A) modification, as one of the most common types of internal modifications of RNA in eukaryotes, exerts a multifunctional role in physiological and pathological processes by regulating the metabolism of RNA. With the in-depth understanding and research of fibrosis, we found that m6A modification plays an important role in fibrosis, and m6A regulators can further participate in the pathophysiological process of fibrosis by regulating the function of specific cells. In our review, we summarized the latest research advances in m6A modification in fibrosis, as well as the specific functions of different m6A regulators. In addition, we focused on the mechanisms and roles of m6A modification in cardiac fibrosis, liver fibrosis, pulmonary fibrosis, renal fibrosis, retinal fibrosis and oral submucosal fibrosis, with the aim of providing new insights and references for finding potential therapeutic targets for fibrosis. Finally, we discussed the prospects and challenges of targeted m6A modification in the treatment of fibrotic diseases.
引用
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页数:13
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