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RNA N6-甲基腺嘌呤修饰在创面修复相关病理生理进程中的作用研究进展

刘笑笑 刘德伍

刘笑笑, 刘德伍. RNA N6-甲基腺嘌呤修饰在创面修复相关病理生理进程中的作用研究进展[J]. 中华烧伤与创面修复杂志, 2022, 38(10): 989-993. DOI: 10.3760/cma.j.cn501120-20210804-00267.
引用本文: 刘笑笑, 刘德伍. RNA N6-甲基腺嘌呤修饰在创面修复相关病理生理进程中的作用研究进展[J]. 中华烧伤与创面修复杂志, 2022, 38(10): 989-993. DOI: 10.3760/cma.j.cn501120-20210804-00267.
Liu XX,Liu DW.Research advances on the effects of RNA N6-methyladenosine modification in the relevant pathophysiological processes of wound repair[J].Chin J Burns Wounds,2022,38(10):989-993.DOI: 10.3760/cma.j.cn501120-20210804-00267.
Citation: Liu XX,Liu DW.Research advances on the effects of RNA N6-methyladenosine modification in the relevant pathophysiological processes of wound repair[J].Chin J Burns Wounds,2022,38(10):989-993.DOI: 10.3760/cma.j.cn501120-20210804-00267.

RNA N6-甲基腺嘌呤修饰在创面修复相关病理生理进程中的作用研究进展

doi: 10.3760/cma.j.cn501120-20210804-00267
基金项目: 

国家自然科学基金地区科学基金项目 81860340, 82160378

详细信息
    通讯作者:

    刘德伍,Email:dewuliu@126.com

Research advances on the effects of RNA N6-methyladenosine modification in the relevant pathophysiological processes of wound repair

Funds: 

Regional Science Fund Project of National Natural Science Foundation of China 81860340, 82160378

More Information
  • 摘要: N6-甲基腺嘌呤(m6A)作为一种转录后修饰广泛存在于真核生物中,该种修饰受到甲基转移酶和去甲基化酶的动态可逆性调控,并通过m6A结合蛋白参与调节生物学效应。近来研究表明,m6A可参与胚胎皮肤形态发生、创面修复以及炎症反应、血管生成和纤维化等病理生理过程。该文概述了m6A及其相关蛋白在创面修复相关病理生理进程中的作用,以期为创面修复的治疗策略提供新的理论依据。

     

  • 参考文献(40)

    [1] HuangH,WengH,ChenJ.m6A modification in coding and non-coding RNAs: roles and therapeutic implications in cancer[J].Cancer Cell,2020,37(3):270-288.DOI: 10.1016/j.ccell.2020.02.004.
    [2] HePC,HeC.m6A RNA methylation: from mechanisms to therapeutic potential[J].EMBO J,2021,40(3):e105977.DOI: 10.15252/embj.2020105977.
    [3] DominissiniD,Moshitch-MoshkovitzS,SchwartzS,et al.Topology of the human and mouse m6A RNA methylomes revealed by m6A-seq[J].Nature,2012,485(7397):201-206.DOI: 10.1038/nature11112.
    [4] MeyerKD,SaletoreY,ZumboP,et al.Comprehensive analysis of mRNA methylation reveals enrichment in 3' UTRs and near stop codons[J].Cell,2012,149(7):1635-1646.DOI: 10.1016/j.cell.2012.05.003.
    [5] FangX,LiM,YuT,et al.Reversible N6-methyladenosine of RNA: the regulatory mechanisms on gene expression and implications in physiology and pathology[J].Genes Dis,2020,7(4):585-597.DOI: 10.1016/j.gendis.2020.06.011.
    [6] ShiH,WeiJ,HeC.Where, when, and how: context-dependent functions of RNA methylation writers, readers, and erasers[J].Mol Cell,2019,74(4):640-650.DOI: 10.1016/j.molcel.2019.04.025.
    [7] YangY,HsuPJ,ChenYS,et al.Dynamic transcriptomic m6A decoration: writers, erasers, readers and functions in RNA metabolism[J].Cell Res,2018,28(6):616-624.DOI: 10.1038/s41422-018-0040-8.
    [8] XiL,CarrollT,MatosI,et al.m6A RNA methylation impacts fate choices during skin morphogenesis[J].Elife,2020,9:e56980.DOI: 10.7554/eLife.56980.
    [9] VeltriA,LangC,LienWH.Concise review: Wnt signaling pathways in skin development and epidermal stem cells[J].Stem Cells,2018,36(1):22-35.DOI: 10.1002/stem.2723.
    [10] LeeJ,WuY,HaradaBT,et al.N6-methyladenosine modification of lncRNA Pvt1 governs epidermal stemness[J].EMBO J,2021,40(8):e106276.DOI: 10.15252/embj.2020106276.
    [11] RodriguesM,KosaricN,BonhamCA,et al.Wound healing: a cellular perspective[J].Physiol Rev,2019,99(1):665-706.DOI: 10.1152/physrev.00067.2017.
    [12] WangJ,YanS,LuH,et al.METTL3 attenuates LPS-induced inflammatory response in macrophages via NF-κB signaling pathway[J].Mediators Inflamm,2019,2019:3120391.DOI: 10.1155/2019/3120391.
    [13] ZhangY,GuX,LiD,et al.METTL3 regulates osteoblast differentiation and inflammatory response via Smad signaling and MAPK signaling[J].Int J Mol Sci,2019,21(1):199.DOI: 10.3390/ijms21010199.
    [14] ZongX,ZhaoJ,WangH,et al.Mettl3 deficiency sustains long-chain fatty acid absorption through suppressing Traf6-dependent inflammation response[J].J Immunol,2019,202(2):567-578.DOI: 10.4049/jimmunol.1801151.
    [15] FengZ,LiQ,MengR,et al.METTL3 regulates alternative splicing of MyD88 upon the lipopolysaccharide-induced inflammatory response in human dental pulp cells[J].J Cell Mol Med,2018,22(5):2558-2568.DOI: 10.1111/jcmm.13491.
    [16] JianD,WangY,JianL,et al.METTL14 aggravates endothelial inflammation and atherosclerosis by increasing FOXO1 N6-methyladeosine modifications[J].Theranostics,2020,10(20):8939-8956.DOI: 10.7150/thno.45178.
    [17] DuJ,LiaoW,LiuW,et al.N6-adenosine methylation of Socs1 mRNA is required to sustain the negative feedback control of macrophage activation[J].Dev Cell,2020,55(6):737-753.e7.DOI: 10.1016/j.devcel.2020.10.023.
    [18] HouJ,ZhangH,LiuJ,et al.YTHDF2 reduction fuels inflammation and vascular abnormalization in hepatocellular carcinoma[J].Mol Cancer,2019,18(1):163.DOI: 10.1186/s12943-019-1082-3.
    [19] MapperleyC,van de LagemaatLN,LawsonH,et al.The mRNA m6A reader YTHDF2 suppresses proinflammatory pathways and sustains hematopoietic stem cell function[J].J Exp Med,2021,218(3):e20200829.DOI: 10.1084/jem.20200829.
    [20] YuR,LiQ,FengZ,et al.m6A reader YTHDF2 regulates LPS-induced inflammatory response[J].Int J Mol Sci,2019,20(6):1323.DOI: 10.3390/ijms20061323.
    [21] ZhengL,TangX,LuM,et al.microRNA-421-3p prevents inflammatory response in cerebral ischemia/reperfusion injury through targeting m6A reader YTHDF1 to inhibit p65 mRNA translation[J].Int Immunopharmacol,2020,88:106937.DOI: 10.1016/j.intimp.2020.106937.
    [22] ZhaoJ,HanDX,WangCB,et al.Zbtb7b suppresses aseptic inflammation by regulating m6A modification of IL6 mRNA[J].Biochem Biophys Res Commun,2020,530(1):336-341.DOI: 10.1016/j.bbrc.2020.07.011.
    [23] WuC,ChenW,HeJ,et al.Interplay of m6A and H3K27 trimethylation restrains inflammation during bacterial infection[J].Sci Adv,2020,6(34):eaba0647.DOI: 10.1126/sciadv.aba0647.
    [24] ChenL,ChengL,ChenT,et al.Macrophage polarization in skin wound healing: progress in biology and therapeutics[J].J Shanghai Jiaotong Univ (Sci),2021,27:264-280.DOI: 10.1007/s12204-021-2276-6.
    [25] GuX,ZhangY,LiD,et al.N6-methyladenosine demethylase FTO promotes M1 and M2 macrophage activation[J].Cell Signal,2020,69:109553.DOI: 10.1016/j.cellsig.2020.109553.
    [26] LiuY,LiuZ,TangH,et al.The N6-methyladenosine (m6A)-forming enzyme METTL3 facilitates M1 macrophage polarization through the methylation of STAT1 mRNA[J].Am J Physiol Cell Physiol,2019,317(4):C762-C775.DOI: 10.1152/ajpcell.00212.2019.
    [27] WangQ,ChenC,DingQ,et al.METTL3-mediated m6A modification of HDGF mRNA promotes gastric cancer progression and has prognostic significance[J].Gut,2020,69(7):1193-1205.DOI: 10.1136/gutjnl-2019-319639.
    [28] YangZ,WangT,WuD,et al.RNA N6-methyladenosine reader IGF2BP3 regulates cell cycle and angiogenesis in colon cancer[J].J Exp Clin Cancer Res,2020,39(1):203.DOI: 10.1186/s13046-020-01714-8.
    [29] WangLJ,XueY,LiH,et al.Wilms' tumour 1-associating protein inhibits endothelial cell angiogenesis by m6A-dependent epigenetic silencing of desmoplakin in brain arteriovenous malformation[J].J Cell Mol Med,2020,24(9):4981-4991.DOI: 10.1111/jcmm.15101.
    [30] MathiyalaganP,AdamiakM,MayourianJ,et al.FTO-dependent N6-methyladenosine regulates cardiac function during remodeling and repair[J].Circulation,2019,139(4):518-532.DOI: 10.1161/CIRCULATIONAHA.118.033794.
    [31] ShanK,ZhouRM,XiangJ,et al.FTO regulates ocular angiogenesis via m6A-YTHDF2-dependent mechanism[J].Exp Eye Res,2020,197:108107.DOI: 10.1016/j.exer.2020.108107.
    [32] WangLJ,XueY,HuoR,et al.N6-methyladenosine methyltransferase METTL3 affects the phenotype of cerebral arteriovenous malformation via modulating Notch signaling pathway[J].J Biomed Sci,2020,27(1):62.DOI: 10.1186/s12929-020-00655-w.
    [33] YaoMD,JiangQ,MaY,et al.Role of METTL3-dependent N6-methyladenosine mRNA modification in the promotion of angiogenesis[J].Mol Ther,2020,28(10):2191-2202.DOI: 10.1016/j.ymthe.2020.07.022.
    [34] LiuSY,WuJJ,ChenZH,et al.The m6A RNA modification modulates gene expression and fibrosis-related pathways in hypertrophic scar[J].Front Cell Dev Biol,2021,9:748703.DOI: 10.3389/fcell.2021.748703.
    [35] LiT,ZhuangY,YangW,et al.Silencing of METTL3 attenuates cardiac fibrosis induced by myocardial infarction via inhibiting the activation of cardiac fibroblasts[J].FASEB J,2021,35(2):e21162.DOI: 10.1096/fj.201903169R.
    [36] LinX,ChaiG,WuY,et al.RNA m6A methylation regulates the epithelial mesenchymal transition of cancer cells and translation of Snail[J].Nat Commun,2019,10(1):2065.DOI: 10.1038/s41467-019-09865-9.
    [37] TangB,YangY,KangM,et al.m6A demethylase ALKBH5 inhibits pancreatic cancer tumorigenesis by decreasing WIF-1 RNA methylation and mediating Wnt signaling[J].Mol Cancer,2020,19(1):3.DOI: 10.1186/s12943-019-1128-6.
    [38] NingY,ChenJ,ShiY,et al.Genistein ameliorates renal fibrosis through regulation snail via m6A RNA demethylase ALKBH5[J].Front Pharmacol,2020,11:579265.DOI: 10.3389/fphar.2020.579265.
    [39] HanB,ChuC,SuX,et al.N6-methyladenosine-dependent primary microRNA-126 processing activated PI3K-AKT-mTOR pathway drove the development of pulmonary fibrosis induced by nanoscale carbon black particles in rats[J].Nanotoxicology,2020,14(1):1-20.DOI: 10.1080/17435390.2019.1661041.
    [40] LiuP,ZhangB,ChenZ,et al.m6A-induced lncRNA MALAT1 aggravates renal fibrogenesis in obstructive nephropathy through the miR-145/FAK pathway[J].Aging (Albany NY),2020,12(6):5280-5299.DOI: 10.18632/aging.102950.
  • 1  m6A介导的RNA调控机制示意图

    注:METTL为甲基转移酶样,WTAP为Wilms肿瘤1结合蛋白,KIAAI429为Vir样N6-甲基腺嘌呤(m6A)相关甲基转移酶,ZC3H13为具有CCCH结构锌指蛋白13,RBM15/15B为RNA结合基序蛋白15/15B,ALKBH5为烷基化蛋白AlkB同源物5,FTO为肥胖相关蛋白,HNRNP为核不均一核糖核酸蛋白,YTHDC1为含有YTH结构域1,YTHDF为YTH结构域家族,IGF2BP为胰岛素样生长因子2 mRNA结合蛋白

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出版历程
  • 收稿日期:  2021-08-04
  • 网络出版日期:  2022-10-24

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