microRNA在肾脏疾病和生理中的研究进展
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摘要
慢性肾脏疾病(CKD)与主要的非传染性疾病(如糖尿病和高血压)密切相关。微RNA(miRNA)是一类内源性有调控作用的非编码RNA,它们在肾脏发育、平衡和疾病中扮演重要角色。特别是在各种CKD的发展中,miRNA的表达与肾小管间质硬化和终末期肾小球病变发生相关。miRNA在基因中具有调控作用,其可能成为肾病的一种新的诊断标志物和治疗靶点。根据现有证据,miRNA可能与糖尿病肾病、IgA肾病、狼疮性肾炎、多囊肾病和移植排斥有关。
Chronic kidney disease( CKD) is closely related to non-communicable diseases such as diabetes and hypertension. MicroRNAs( miRNAs) are a class of endogenous,non-encoding RNAs that play an important role in kidney development,homeostasis and disease. In particular,the development of various CKD,miRNA expression is closely related to the occurrence of tubulointerstitial sclerosis and terminal glomerular disease. miRNAs have a regulatory role in genes that may become a new diagnostic marker and therapeutic target for nephropathy. Based on available evidence,miRNAs seem to be associated with diabetic nephropathy,IgA nephropathy,lupus nephritis,polycystic nephropathy and graft rejection.
Chronic kidney disease( CKD) is closely related to non-communicable diseases such as diabetes and hypertension. MicroRNAs( miRNAs) are a class of endogenous,non-encoding RNAs that play an important role in kidney development,homeostasis and disease. In particular,the development of various CKD,miRNA expression is closely related to the occurrence of tubulointerstitial sclerosis and terminal glomerular disease. miRNAs have a regulatory role in genes that may become a new diagnostic marker and therapeutic target for nephropathy. Based on available evidence,miRNAs seem to be associated with diabetic nephropathy,IgA nephropathy,lupus nephritis,polycystic nephropathy and graft rejection.
引文
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[36]Danger R,Pallier A,Giral M,et al.Upregulation of miR-142-3p in peripheral blood mononuclear cells of operationally tolerant patients with a renal transplant[J].Am Soc Nephrol,2012,23(4):597-606.
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[39]Janssen HL,Reesink HW,Lawitz EJ,et al.Treatment of HCV infection by targeting microRNA[J].N Engl J Med,2013,36(8):1685-1694.
[2]Lorenzen JM,Thum T.Circulating and urinary microRNAs in kidney disease[J].Clin J Am Soc Nephrol,2012,7(9):1528-1533.
[3]Ruggenenti P,Cravedi P,Remuzzi G.Mechanisms and treatment of CKD[J].J Am Soc Nephrol,2012,23(12):1917-1928.
[4]Saikumar J,Ramachandran K,Vaidya VS.Noninvasive micromarkers[J].Clin Chem,2014,60(9):1158-1173.
[5]金吉春.microRNA的概述及其研究[J].医学研究生学报,2013,26(10):1109-1112.
[6]李羿,赵洪雯,申兵冰,等.microRNA与肾间质纤维化的研究进展[J].现代生物医学进展,2014,14(24):4794-4797.
[7]Huntzinger E,Izaurralde E.Gene silencing by microRNAs:Contributions of translational repression and mRNA decay[J].Nat Rev Genet,2011,12(2):99-110.
[8]Russo G,Giordano A.miRNAs:From biogenesis to networks[J].Methods Mol Biol,2009,563:303-352.
[9]Zhang Z,Qin YW,Brewer G,et al.MicroRNA degradation and turnover:Regulating the regulators[J].Wiley Interdiscip Rev RNA,2012,3(4):593-600.
[10]Roberts AB,Mccune BK,Sporn B.TGF-bold beta:Regulation of extracellular matrix[J].Kidney Int,1992,41(5):57-59.
[11]He Y,Huang C,Lin X,et al.MicroRNA-29 family,a crucial therapeutic target for fibrosis diseases[J].Biochimie,2013,95(7):1355-1359.
[12]林莉.miRNA-21对大鼠糖尿病肾病TGF-β/Smad信号通路的调控机制研究[D].重庆:重庆医科大学,2014.
[13]张涛,张正彪,阿力木,等.miRNA-200b在肾癌患者血清中的异常表达及其临床意义[J].中国临床研究,2016,29(11):1474-1476.
[14]Wang B,Komers R,Carew R,et al.Suppression of microRNA-29expression by TGF-β1promotes collagen expression and renal fibrosis[J].J Am Soc Nephrol,2012,23(2):252-265.
[15]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.
[16]Jiang F,Liu GS,Dusting GJ,et al.NADPH oxidase-dependent redox signaling in TGF-β-mediated fibrotic responses[J].Redox Biol,2014,2(1):267-272.
[17]López-Hernández FJ,López-Novoa JM.Role of TGF-βin chronic kidney disease:An integration of tubular,glomerular and vascular effects[J].Cell Tissue Res,2012,347(1):141-154.
[18]Inman Gareth J,Nicolás Francisco J,Hill Caroline S.Nucleocytoplasmic shuttling of Smads 2,3,and 4 permits sensing of TGFbeta receptor activity[J].Molecular Cell,2002,102:283-294.
[19]Derynck R,Zhang YE.Smad-dependent and Smad-independent pathways in TGF-beta family signalling[J].Nature,2003,425(6958):577-584.
[20]Butz H,Rácz K,Hunyady L,et al.Crosstalk between TGF-βsignaling and the microRNA machinery[J].Trends Pharmacol Sci,2012,33(7):382-393.
[21]Qin W,Chung AC,Huang XR,et al.TGF-β/Smad3 signaling promotes renal fibrosis by inhibiting miR-29[J].J Am Soc Nephrol,2011,22(8):1462-1474.
[22]刘洁,侯明辉,刘莉,等.EGR-1基因转染对高糖环境中小鼠肾小球系膜细胞TGF-β及PDGF-B表达的影响[J].中国免疫学杂志,2012,28(6):497-501.
[23]Wang Q,Wang Y,Minto AW,et al.MicroRNA377 is up-regulated and can lead to increased fibronectin production in diabetic nephropathy[J].FASEB J,2008,22(12):4126-4135.
[24]Tang O,Chen XM,Shen S,et al.MiRNA200b represses transforming growth factorβ1-induced EMT and fibronectin expression in kidney proximal tubular cells[J].Am J Physiol Renal Physiol,2013,30(4):1266-1273.
[25]Jiang L,Qiu WJ,Zhou Y,et al.A microRNA30e/mitochondrial uncoupling protein 2 axis mediates TGF-β1-induced tubular epithelial cell extracellular matrix production and kidney fibrosis[J].Kidney Int,2013,84(8):285-296.
[26]Park JT,Kato M,Yuan H,et al.FOG2 protein down-regulation by transforming growth factor-β1-induced microRNA-200b/c leads to Akt kinase activation and glomerular mesangial hypertrophy related to diabetic nephropathy[J].J Biol Chem,2013,288(31):22469-22480.
[27]Zhou H,Hasni SA,Perez P,et al.miR-150 promotes renal fibrosis in lupus nephritis by downregulating SOCS1[J].J Am Soc Nephrol,2013,24(7):1073-1087.
[28]Serino G,Sallustio F,Cox SN,et al.Abnormal miR-148b expression promotes aberrant glycosylation of Ig A1 in Ig A nephropathy[J].J Am Soc Nephrol,2012,23(5):814-824.
[29]Bao H,Chen H,Zhu XD,et al.MiR-223 downregulation promotes glomerular endothelial cell activation by upregulating importinα4 andα5 in Ig A nephropathy[J].Kidney Int,2014,85(3):624-635.
[30]Elvira-Matelot E,Zhou XO,Farman N,et al.Regulation of WNK1expression by miR192 and aldosterone[J].J Am Soc Nephrol,2010,21(10):1724-1731.
[31]Yamagishi S,Fukami K,Ueda S,et al.Molecular mechanisms of diabetic nephropathy and its therapeutic intervention[J].Current Drug Targets,2007,8(8):952-959.
[32]Qian Y,Feldman E,Pennathur S,et al.From fibrosis to sclerosis:Mechanisms of glomerulosclerosis in diabetic nephropathy[J].Diabetes,2008,57(6):1439-1445.
[33]Long J,Wang Y,Wang W,et al.MicroRNA-29c is a signature microRNA under high glucose conditions that targets Sprouty homolog 1,and its in vivo knockdown prevents progression of diabetic nephropathy[J].Biol Chem,2011,286(13):11837-11848.
[34]Anglicheau D,Sharma VK,Ding R,et al.MicroRNA expression profiles predictive of human renal allograft status[J].Proc Natl Acad Sci U S A,2009,106(13):5330-5335.
[35]Wilflingseder J,Regele H,Perco P,et al.miRNA profiling discriminates types of rejection and injury in human renal allografts[J].Transplantation,2013,95(6):835-841.
[36]Danger R,Pallier A,Giral M,et al.Upregulation of miR-142-3p in peripheral blood mononuclear cells of operationally tolerant patients with a renal transplant[J].Am Soc Nephrol,2012,23(4):597-606.
[37]Scian MJ,Maluf DG,David KG,et al.MicroRNA Profiles in allograft tissues and paired urines associate with chronic allograft dysfunction with IF/TA[J].Am J Transplant,2011,11(10):2110-2122.
[38]Maluf DG,Dumur CI,Suh JL,et al.The urine microRNA profile may help monitor post-transplant renal graft function[J].Kidney Int,2014,85(2):439-449.
[39]Janssen HL,Reesink HW,Lawitz EJ,et al.Treatment of HCV infection by targeting microRNA[J].N Engl J Med,2013,36(8):1685-1694.
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