microRNA在糖尿病肾病发病机制中的研究进展
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摘要
微小RNA (miRNA)为人类新发现的一类具有调控人体多蛋白基因组学作用的非编码RNA,在与靶基因位点互补与配对结合后,通过对转录后调控靶基因表达参与机体各种生理与病理过程的调节作用,调控细胞活化、增殖、分化、凋亡以及生物体生长、发育,对机体免疫反应及疾病的发生发展与转归起到了重要的调控作用。目前microRNA成为生命科学研究的热点之一,MicroRNA在糖尿病肾病(DN)发病机制中的调节作用日益受到关注,研究发现,MicroRNA对肾小球基底膜和系膜的损伤、足细胞的损伤及肾间质纤维化的调控方面都起到了关键作用。
MicroRNA(MicroRNA, microRNA) is a new type of non-coding RNA that has been found to regulate human polyproteomics. After complementation and pairing with target gene sites, microRNA participates in the regulation of various physiological and pathological processes by regulating the expression of target genes after transcription,and regulates cell activation, proliferation, differentiation, apoptosis, growth and development of organisms, which plays important regulatory roles in immune response, the occurrence, development and prognosis of diseases. At present, micro RNA has become one of the hotspots of life science research, and the regulatory role of micro RNA in the pathogenesis of diabetic nephropathy(DN) has attracted increasing attention. It has been found that micro RNA plays a key role in the regulation of glomerular basement membrane and mesangium damage, podocyte damage, and renal interstitial fibrosis.
MicroRNA(MicroRNA, microRNA) is a new type of non-coding RNA that has been found to regulate human polyproteomics. After complementation and pairing with target gene sites, microRNA participates in the regulation of various physiological and pathological processes by regulating the expression of target genes after transcription,and regulates cell activation, proliferation, differentiation, apoptosis, growth and development of organisms, which plays important regulatory roles in immune response, the occurrence, development and prognosis of diseases. At present, micro RNA has become one of the hotspots of life science research, and the regulatory role of micro RNA in the pathogenesis of diabetic nephropathy(DN) has attracted increasing attention. It has been found that micro RNA plays a key role in the regulation of glomerular basement membrane and mesangium damage, podocyte damage, and renal interstitial fibrosis.
引文
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[14]Duan LJ,Qi J,Kong XJ,et al.MiR-133 modulates TGF-β1-induced bladder smooth muscle cell hypertrophic and fibrotic response:implication for a role of microRNA in bladder wall remodeling caused by bladder outlet obstruction[J].Cell Signal,2015,27(2):215-227.
[15]Wang Y,Fu B,Sun X,et al.Differentially expressed microRNAs in bone marrow mesenchymal stem cell-derived microvesicles in young and older rats and their effect on tumor growth factor-β1-mediated epithelial-mesenchymal transition in HK2 cells[J].Stem Cell Res Ther,2015,6:185.
[16]曹聃,孙雪峰.MicroRNA在肾组织纤维化中的研究进展[J].中国实用内科杂志,2017,37(3):262-264.
[17]JOHNSON CD,ESQUELA-KERSCHER A,STEFANI G,et al.The let-7 microRNA represses cell proliferation pathways in human cells[J].Cancer Res,2007,67(16):7713-7722.
[18]MATSUURA K,DE GIORGI V,SCHECHTERLY C,et al.Circulating let-7 levels in plasma and extracellular vesicles correlate with hepatic fibrosis progression in chronic hepatitis C[J].Hepatology,2016,64(3):732-745.
[19]WANG B,JHA JC,HAGIWARA S,et al.Transforming growth factor-β1-mediated renal fibrosis is dependent on the regulation of transforming growth factor receptor 1 expression by let-7b[J].Kidney Int,2014,85(2):352-361.
[20]XIONG M,JIANG L,ZHOU Y,et al.The miR-200 family regulates TGF-β1-induced renal tubular epithelial to mesenchymal transition through Smad pathway by targeting ZEB1 and ZEB2 expression[J].Am J Physiol Renal Physiol,2012,302(3):F369-F379.
[21]张永,徐焱成.Micro RNA与DM肾病的研究进展[J].湖北医药学院学报,2014,33(3):306-309.
[22]HUANG Y,TONG J,HE F,et al.miR-141 regulates TGF-β1-induced epithelial-mesenchymal transition through repression of HIPK2 expression in renal tubular epithelial cells[J].Int J Mol Med,2015,35(2):311-318.
[23]ZHONG X,CHUNG AC,CHEN HY,et al.miR-21 is a key therapeutic target for renal injury in a mouse model of type 2 diabetes[J].Diabetologia,2013,56(3):663-674.
[24]XU X,KRIEGEL AJ,LIU Y,et al.Delayed ischemic preconditioning contributes to renal protection by upregulation of miR-21[J].Kidney Int,2012,82(11):1167-1175.
[25]MCCLELLAND AD,HERMAN-EDELSTEIN M,KOMERS R,et al.miR-21 promotes renal fibrosis in diabetic nephropathy by targeting PTEN and SMAD7[J].Clin Sci(Lond),2015,129(12):1237-1249.
[26]WANG JY,GAO YB,ZHANG N,et al.miR-21 overexpression enhances TGF-β1-induced epithelial-to-mesenchymal transition by target smad7 and aggravates renal damage in diabetic nephropathy[J].Mol Cell Endocrinol,2014,392(1-2):163-172.
[2]REUTENS AT,ATKINS RC.Epidemiology of diabetic nephropathy[J].Contrib Nephrol,2011,170:1-7.
[3]MACISAAC RJ,EKINCI EI,JERUMS G.Markers of and risk factors for the development and progression of diabetic kidney disease[J].Am J Kidney Dis,2014,63(2 Suppl 2):S39-S62.
[4]LEE RC,FEINBAUM RL,AMBROS V.The C.elegans heterochronic gene lin-4 encodes small RNAs with antisense complementarity to lin-14[J].Cell,1993,75(5):843-854.
[5]李香,王丽宏,傅雪莲,等.microRNA在DM肾病中的作用.东南大学学报(医学版),2015,34(2):325-328.
[6]王晓莉,覃建阳,滕玲,等.MicroRNA与DM肾病[J].解剖科学进展,2014,20(6):567-570.
[7]WANG T,CHEN SS,CHEN R,et al.Reduced beta 2 glycoprotein Iimproves diabetic nephropathy via inhibiting TGF-β1-p38 MAPKpathway[J].Int J Clin Exp Pathol,2015,8(3):2321-2333.
[8]XU ZJ,SHU S,LI ZJ,et al.Liuwei Dihuang pill treats diabetic nephropathy in rats by inhibiting of TGF-β/SMADS,MAPK,and NF-κBand upregulating expression of cytoglobin in renal tissues[J].Medicine(Baltimore),2017,96(3):e5879.
[9]WANG Y,LE Y,XUE JY,et al.Let-7d miRNA prevents TGF-β1-induced EMT and renal fibrogenesis through regulation of HMGA2 expression[J].Biochem Biophys Res Commun,2016,479(4):676-682.
[10]LEE HW,KHAN SQ,KHALIQDINA S,et al.Absence of miR-146a in podocytes increases risk of diabetic glomerulopathy via up-regulation of ErbB4 and Notch-1[J].J Biol Chem,2017,292(2):732-747.
[11]谢沂均,张倩,薛耀明.microRNA在DM肾病小管间质纤维化中的作用[J].肾脏病与透析肾移植杂志,2017,26(5):457-459.
[12]HAQUE R,IUVONE PM,HE L,et al.The MicroRNA-21 signaling pathway is involved in prorenin receptor(PRR)-induced VEGF expression in ARPE-19 cells under a hyperglycemic condition[J].Mol Vis,2017,23:251-262.
[13]覃宁玲,盛德乔.microRNA与DM肾病关系的研究进展[J].广东医学,2015,36(9):1446-1449.
[14]Duan LJ,Qi J,Kong XJ,et al.MiR-133 modulates TGF-β1-induced bladder smooth muscle cell hypertrophic and fibrotic response:implication for a role of microRNA in bladder wall remodeling caused by bladder outlet obstruction[J].Cell Signal,2015,27(2):215-227.
[15]Wang Y,Fu B,Sun X,et al.Differentially expressed microRNAs in bone marrow mesenchymal stem cell-derived microvesicles in young and older rats and their effect on tumor growth factor-β1-mediated epithelial-mesenchymal transition in HK2 cells[J].Stem Cell Res Ther,2015,6:185.
[16]曹聃,孙雪峰.MicroRNA在肾组织纤维化中的研究进展[J].中国实用内科杂志,2017,37(3):262-264.
[17]JOHNSON CD,ESQUELA-KERSCHER A,STEFANI G,et al.The let-7 microRNA represses cell proliferation pathways in human cells[J].Cancer Res,2007,67(16):7713-7722.
[18]MATSUURA K,DE GIORGI V,SCHECHTERLY C,et al.Circulating let-7 levels in plasma and extracellular vesicles correlate with hepatic fibrosis progression in chronic hepatitis C[J].Hepatology,2016,64(3):732-745.
[19]WANG B,JHA JC,HAGIWARA S,et al.Transforming growth factor-β1-mediated renal fibrosis is dependent on the regulation of transforming growth factor receptor 1 expression by let-7b[J].Kidney Int,2014,85(2):352-361.
[20]XIONG M,JIANG L,ZHOU Y,et al.The miR-200 family regulates TGF-β1-induced renal tubular epithelial to mesenchymal transition through Smad pathway by targeting ZEB1 and ZEB2 expression[J].Am J Physiol Renal Physiol,2012,302(3):F369-F379.
[21]张永,徐焱成.Micro RNA与DM肾病的研究进展[J].湖北医药学院学报,2014,33(3):306-309.
[22]HUANG Y,TONG J,HE F,et al.miR-141 regulates TGF-β1-induced epithelial-mesenchymal transition through repression of HIPK2 expression in renal tubular epithelial cells[J].Int J Mol Med,2015,35(2):311-318.
[23]ZHONG X,CHUNG AC,CHEN HY,et al.miR-21 is a key therapeutic target for renal injury in a mouse model of type 2 diabetes[J].Diabetologia,2013,56(3):663-674.
[24]XU X,KRIEGEL AJ,LIU Y,et al.Delayed ischemic preconditioning contributes to renal protection by upregulation of miR-21[J].Kidney Int,2012,82(11):1167-1175.
[25]MCCLELLAND AD,HERMAN-EDELSTEIN M,KOMERS R,et al.miR-21 promotes renal fibrosis in diabetic nephropathy by targeting PTEN and SMAD7[J].Clin Sci(Lond),2015,129(12):1237-1249.
[26]WANG JY,GAO YB,ZHANG N,et al.miR-21 overexpression enhances TGF-β1-induced epithelial-to-mesenchymal transition by target smad7 and aggravates renal damage in diabetic nephropathy[J].Mol Cell Endocrinol,2014,392(1-2):163-172.