[1]孙崇凯,杨炎林,高林,等.m6A甲基化在2型糖尿病及其并发症中的重要作用[J].国际内分泌代谢杂志,2021,41(04):368-371.[doi:10.3760/cma.j.cn121383-20210304-03009]
 Sun Chongkai,Yang Yanlin,Gao Lin,et al.The critical role of m6A methylation in type 2 diabetes mellitus and its complications[J].International Journal of Endocrinology and Metabolism,2021,41(04):368-371.[doi:10.3760/cma.j.cn121383-20210304-03009]
点击复制

m6A甲基化在2型糖尿病及其并发症中的重要作用()
分享到:

《国际内分泌代谢杂志》[ISSN:1673-4157/CN:12-1383/R]

卷:
41
期数:
2021年04期
页码:
368-371
栏目:
综述
出版日期:
2021-07-20

文章信息/Info

Title:
The critical role of m6A methylation in type 2 diabetes mellitus and its complications
作者:
孙崇凯1杨炎林2高林1薛耀明2
1南方医科大学第一临床医学院,广州 510515; 2南方医科大学南方医院内分泌代谢病科,广州 510515
Author(s):
Sun Chongkai1 Yang Yanlin2 Gao Lin1 Xue Yaoming2.
1The First Clinical Medical Institute, Southern Medical University, Guangzhou 510515, China; 2Department of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China
关键词:
2型糖尿病 并发症 RNA 甲基化 N6-甲基腺苷
Keywords:
Type 2 diabetes mellitus Complications RNA methylation N6-methyladenosine
DOI:
10.3760/cma.j.cn121383-20210304-03009
摘要:
目前2型糖尿病(T2DM)及其并发症的发病机制仍未研究清楚。近年来一些报道表明,表观遗传学可能在T2DM及其并发症的发生、发展中起到重要作用,而N6-甲基腺苷(m6A)是真核生物中存在的RNA分子最普遍和最丰富的修饰之一。探讨m6A甲基化与T2DM及其并发症之间的关系可以为疾病的诊断和治疗提供更多的可能性,通过一些针对甲基转移酶和脱甲基酶的特异性抑制剂来选择性地调节m6A修饰对于治疗可能有利。
Abstract:
At present, pathogenesis of the type 2 diabetes mellitus(T2DM)and its complications remain unclear. In recent years, some reports indicate that epigenetics may play an essential role in the occurrence and development of T2DM and its complications, and mRNA N6-methyladenosine(m6A)is one of the most common and abundant modifications of RNA molecules in eukaryotes. Exploring the relationship between the methylation of m6A and T2DM and its complications can provide more possibilities for the diagnosis and treatment of the disease. It may be beneficial for the treatment to selectively regulate the modification of m6A by some specific inhibitors of methyltransferase and demethylase.

参考文献/References:

[1] Pinhas-Hamiel O,Zeitler P.Acute and chronic complications of type 2 diabetes mellitus in children and adolescents[J].Lancet,2007,369(9575):1823-1831.DOI:10.1016/S0140-6736(07)60821-6.
[2] Wang X,Feng J,Xue Y,et al.Structural basis of N(6)-adenosine methylation by the METTL3-METTL14 complex[J].Nature,2016,534(7608):575-578.DOI:10.1038/nature18298.
[3] Ping XL,Sun BF,Wang L,et al.Mammalian WTAP is a regulatory subunit of the RNA N6-methyladenosine methyltransferase[J].Cell Res,2014,24(2):177-189.DOI:10.1038/cr.2014.3.
[4] Fu Y,Jia G,Pang X,et al.FTO-mediated formation of N6-hydroxymethyladenosine and N6-formyladenosine in mammalian RNA[J].Nat Commun,2013,4:1798.DOI:10.1038/ncomms2822.
[5] Zheng G,Dahl JA,Niu Y,et al.ALKBH5 is a mammalian RNA demethylase that impacts RNA metabolism and mouse fertility[J].Mol Cell,2013,49(1):18-29.DOI:10.1016/j.molcel.2012.10.015.
[6] Wang X,Zhao BS,Roundtree IA,et al.N6-methyladenosine modulates messenger RNA translation efficiency[J].Cell,2015,161(6):1388-1399.DOI:10.1016/j.cell.2015.05.014.
[7] Wang X,Lu Z,Gomez A,et al.N6-methyladenosine-dependent regulation of messenger RNA stability[J].Nature,2014,505(7481):117-120.DOI:10.1038/nature12730.
[8] Shi H,Wang X,Lu Z,et al.YTHDF3 facilitates translation and decay of N6-methyladenosine-modified RNA[J].Cell Res,2017,27(3):315-328.DOI:10.1038/cr.2017.15.
[9] Xiao W,Adhikari S,Dahal U,et al.Nuclear m(6)A reader YTHDC1 regulates mRNA splicing[J].Mol Cell,2016,61(4):507-519.DOI:10.1016/j.molcel.2016.01.012.
[10] Hsu PJ,Zhu Y,Ma H,et al.Ythdc2 is an N6-methyladenosine binding protein that regulates mammalian spermatogenesis[J].Cell Res,2017,27(9):1115-1127.DOI:10.1038/cr.2017.99.
[11] De Jesus DF,Zhang Z,Kahraman S,et al.m6A mRNA methylation regulates human β-cell biology in physiological states and in type 2 diabetes[J].Nat Metab,2019,1(8):765-774.DOI:10.1038/s42255-019-0089-9.
[12] Guo S,Dai C,Guo M,et al.Inactivation of specific β cell transcription factors in type 2 diabetes[J].J Clin Invest,2013,123(8):3305-3316.DOI:10.1172/JCI65390.
[13] Liu J,Luo G,Sun J,et al.METTL14 is essential for β-cell survival and insulin secretion[J].Biochim Biophys Acta Mol Basis Dis,2019,1865(9):2138-2148.DOI:10.1016/j.bbadis.2019.04.011.
[14] Li X,Jiang Y,Sun X,et al.METTL3 is required for maintaining β-cell function[J].Metabolism,2021,116:154702.DOI:10.1016/j.metabol.2021.154702.
[15] Shen F,Huang W,Huang JT,et al.Decreased N(6)-methyladenosine in peripheral blood RNA from diabetic patients is associated with FTO expression rather than ALKBH5[J].J Clin Endocrinol Metab,2015,100(1):E148-E154.DOI:10.1210/jc.2014-1893.
[16] Farah BL,Landau DJ,Sinha RA,et al.Induction of autophagy improves hepatic lipid metabolism in glucose-6-phosphatase deficiency[J].J Hepatol,2016,64(2):370-379.DOI:10.1016/j.jhep.2015.10.008.
[17] Samuel VT,Shulman GI.The pathogenesis of insulin resistance:integrating signaling pathways and substrate flux[J].J Clin Invest,2016,126(1):12-22.DOI:10.1172/JCI77812.
[18] Zhou B,Liu C,Xu L,et al.N6-methyladenosine reader protein YT521-B homology domain-containing 2 suppresses liver steatosis by regulation of mRNA stability of lipogenic genes[J].Hepatology,2021,73(1):91-103.DOI:10.1002/hep.31220.
[19] Yang J,Liu J,Zhao S,et al.N6-methyladenosine METTL3 modulates the proliferation and apoptosis of lens epithelial cells in diabetic cataract[J].Mol Ther Nucleic Acids,2020,20:111-116.DOI:10.1016/j.omtn.2020.02.002.
[20] Zha X,Xi X,Fan X,et al.Overexpression of METTL3 attenuates high-glucose induced RPE cell pyroptosis by regulating miR-25-3p/PTEN/Akt signaling cascade through DGCR8[J].Aging(Albany NY),2020,12(9):8137-8150.DOI:10.18632/aging.103130.
[21] Guo M,Liu D,Sha Q,et al.Succinic acid enhanced quantitative determination of blood modified nucleosides in the development of diabetic nephropathy based on hydrophilic interaction liquid chromatography mass spectrometry[J].J Pharm Biomed Anal,2019,164:309-316.DOI:10.1016/j.jpba.2018.10.042.
[22] Xu Z,Jia K,Wang H,et al.METTL14-regulated PI3K/Akt signaling pathway via PTEN affects HDAC5-mediated epithelial-mesenchymal transition of renal tubular cells in diabetic kidney disease[J].Cell Death Dis,2021,12(1):32.DOI:10.1038/s41419-020-03312-0.

相似文献/References:

[1]曾静波,王姮.2型糖尿病与自身免疫反应[J].国际内分泌代谢杂志,2007,(04):259.
[2]朱素君,谢锦桃,刘军,等.二甲双胍:2型糖尿病治疗的基础药[J].国际内分泌代谢杂志,2007,(04):280.
[3]刘艳清 易秋艳 邵加庆.肠道菌群与肥胖和糖尿病的关系[J].国际内分泌代谢杂志,2015,(01):31.[doi:DOI:10.3760/cma.j.issn.1673-4157.2015.01.007]
 Liu Yanqing,Yi Qiuyan,Shao Jiaqing..Relationship between gut microbiota, obesity and diabetes[J].International Journal of Endocrinology and Metabolism,2015,(04):31.[doi:DOI:10.3760/cma.j.issn.1673-4157.2015.01.007]
[4]姚旻 赵爱源 张宏.肠道菌群与2型糖尿病[J].国际内分泌代谢杂志,2015,(01):35.[doi:DOI:10.3760/cma.j.issn.1673-4157.2015.01.008]
 Yao Min*,Zhao Aiyuan,Zhang Hong..Relationship between gut microbiota and type 2 diabetes[J].International Journal of Endocrinology and Metabolism,2015,(04):35.[doi:DOI:10.3760/cma.j.issn.1673-4157.2015.01.008]
[5]赵丽娟,徐宽枫,杨涛,等.SLC30A8和PTPRD基因多态性与南京地区中老年人群2型糖尿病的相关性研究[J].国际内分泌代谢杂志,2015,(03):145.[doi:10.3760/cma.j.issn.1673-4157.2015.03.001]
 Zhao Lijuan*,Xu Kuanfeng,Yang Tao,et al.Relationship between SLC30A8 and PTPRD gene polymorphisms and type 2 diabetes in middle aged and elderly people in Nanjing area[J].International Journal of Endocrinology and Metabolism,2015,(04):145.[doi:10.3760/cma.j.issn.1673-4157.2015.03.001]
[6]王洁,何媛,于珮.糖尿病肾病的相关危险因素分析[J].国际内分泌代谢杂志,2015,(03):153.[doi:10.3760/cma.j.issn.1673-4157.2015.03.003]
 Wang Jie*,He Yuan,Yu Pei..Risk factors of diabetic nephropathy[J].International Journal of Endocrinology and Metabolism,2015,(04):153.[doi:10.3760/cma.j.issn.1673-4157.2015.03.003]
[7]刘帅,张萍,方毅,等.2型糖尿病合并无症状冠状动脉钙化的相关危险因素分析[J].国际内分泌代谢杂志,2015,(03):158.[doi:10.3760/cma.j.issn.1673-4157.2015.03.004]
 Liu Shuai*,Zhang Ping,Fang Yi,et al.Analysis of the risk factors related with asymptomatic coronary calcification for type 2 diabetic patients[J].International Journal of Endocrinology and Metabolism,2015,(04):158.[doi:10.3760/cma.j.issn.1673-4157.2015.03.004]
[8]徐庆海,马颖,李铁马.2型糖尿病患者高甘油三酯血症-腰围表型与甲状腺功能异常的关系[J].国际内分泌代谢杂志,2015,(04):222.[doi:10.3760/cma.j.issn.1673-4157.2015.04.002]
 Xu Qinghai,Ma Ying,Li Tiema..Association of hypertriglyceridaemic-waist phenotype with thyroid dysfunction in patients with type 2 diabetes mellitus[J].International Journal of Endocrinology and Metabolism,2015,(04):222.[doi:10.3760/cma.j.issn.1673-4157.2015.04.002]
[9]潘道延,沈洁,朱筱,等.利格列汀对2型糖尿病大鼠代谢性内毒素血症的影响[J].国际内分泌代谢杂志,2015,(04):230.[doi:10.3760/cma.j.issn.1673-4157.2015.04.004]
 Pan Daoyan,Shen Jie,Zhu Xiao,et al.Effects of linagliptin on metabolic endotoxemia in type 2 diabetic rats[J].International Journal of Endocrinology and Metabolism,2015,(04):230.[doi:10.3760/cma.j.issn.1673-4157.2015.04.004]
[10]黄桥,白洁,杜洪泉.一种新的脂肪细胞因子——cartonectin[J].国际内分泌代谢杂志,2015,(04):265.[doi:10.3760/cma.j.issn.1673-4157.2015.04.014]
 Huang Qiao*,Bai Jie,Du Hongquan..A novel adipokine--cartonectin[J].International Journal of Endocrinology and Metabolism,2015,(04):265.[doi:10.3760/cma.j.issn.1673-4157.2015.04.014]

备注/Memo

备注/Memo:
通信作者:薛耀明,Email:yaomingxue@126.com
更新日期/Last Update: 1900-01-01