microRNAs在心肌梗死中的研究进展

王丽平

doi:10.13201/j.issn.1001-1439.2016.03.002

microRNAs在心肌梗死中的研究进展

王丽平^,

- 兰州大学第二医院急救中心心电图室(兰州, 730030)

详细信息

通讯作者: 王丽平,E-mail:wlp_lzush@163.com

中图分类号: R542.2

收稿日期: 2015-07-29

Research progress on microRNAs in myocardial infarction

WANG Liping^,

- Electrocardiogram Room, Urgent Care Centre, Second Hospital Affiliated to Lanzhou University, Lanzhou, 730030, China

More Information

Corresponding author: WANG Liping, E-mail: wlp_lzush@163.com

Received Date: 29 July 2015

摘要

摘要: microRNAs(miRNAs)是一种非编码小分子RNA,通过降解mRNA或阻碍其翻译调控基因的表达。心肌梗死是一种常见的心血管疾病,导致心脏重构,最终发展为心力衰竭。miRNAs在心肌梗死的病理生理发展过程中起着重要作用,其可以促进或抑制心肌细胞凋亡,调控心肌细胞增,调节血管再生,此外还能调控心脏成纤维细胞重编程为心肌细胞。本文将综述miRNAs在心肌梗死中的最新进展和治疗前景。
- microRNAs /
- 心肌梗死 /
- 研究进展
Abstract: MicroRNAs (miRNAs) are small noncoding RNAs which could regulate gene expression by translation or induce degradation of mRNA. Myocardial infarction is a common cardiovascular disease that results in cardiac remodeling and leads to the development of heart failure. Several miRNAs have been shown to control important processes of the pathophysiological of myocardial infarction. MiRNAs can promote or inhibit cardiomyocyte cell death, control cardiomyocyte proliferation, and regulate neovascularization. Moreover, miRNAs also involve in the reprogramming of cardiac fibroblasts into cardiomyocytes. In this review, we focus on the current research progress of the role of miRNAs and discuss the therapeutic potential of miRNAs in myocardial infarction.
- microRNAs /
- myocardial Infarction /
- research progress

HTML全文

参考文献(39)

[1]	SMALL E M,FROST R J,OLSON E N.MicroRNAs add a new dimension to cardiovascular disease[J].Circulation,2010,121:1022-1032.
[2]	HULLINGER T G,MONTGOMERY T G,SETO A G,et al.Inhibition of miR-15protects against cardiac ischemic injury[J].Circ Res,2012,110:71-81.
[3]	HERMEKING H.The miR-34family in cancer and apoptosis[J].Cell Death Differ,2010,17:193-199.
[4]	BOON R A,IEKUSHI K,LECHNER S,et al.MicroRNA-34aregulates cardiac ageing and function[J].Nature,2013,495:107-110.
[5]	BERNARDO B C,GAO X M,THAM Y K,et al.Silencing of miR-34aattenuates cardiac dysfunction in a setting of moderate,but not severe,hypertrophic cardiomyopathy[J].PLoS One,2014,9:e90337.
[6]	LI J,LI Y,JIAO J,et al.Mitofusin 1is negatively regulated by microRNA 140in cardiomyocyte apoptosis[J].Mol Cell Biol,2014,34:1788-1799.
[7]	LI R C,TAO J,GUO Y B,et al.In vivo suppression of microRNA-24prevents the transition toward decompensated hypertrophy in aortic-constricted mice[J].Circ.Res,2013,112:601-605.
[8]	AURORA A B,MAHMOUD A I,LUO X,et al.MicroRNA-214protects the mouse heart from ischemic injury by controlling Ca2+overload and cell death[J].J Clin Invest,2012,122:1222-1232.
[9]	LV G,SHAO S,DONG H,et al.MicroRNA-214protects cardiac myocytes against H2O2-induced injury[J].J Cell Biochem,2014,115:93-101.
[10]	PORRELLO E R,OLSON E N.A neonatal blueprint for cardiac regeneration[J].Stem Cell Res,2014,13:556-570.
[11]	PORRELLO E R,MAHMOUD A I,SIMPSON E,et al.Transient regenerative potential of the neonatal mouse heart[J].Science,2011,331:1078-1080.
[12]	PORRELLO E R,JOHNSON B A,AURORA A B,et al.miR-15family regulates postnatal mitotic arrest of cardiomyocytes[J].Circ Res,2011,109:670-679.
[13]	PORRELLO E R,MAHMOUD A I,SIMPSON E,et al.Regulation of neonatal and adult mammalian heart regeneration by the miR-15family[J].Proc Natl Acad Sci USA,2013,110:187-192.
[14]	CHEN J,HUANG Z P,SEOK H Y,et al.miR-17-92cluster is required for and sufficient to induce cardiomyocyte proliferation in postnatal and adult hearts[J].Circ Res,2013,112:1557-1566.
[15]	DANIELSON L S,PARK D S,ROTLLAN N,et al.Cardiovascular dysregulation of miR-17-92causes a lethal hypertrophic cardiomyopathy and arrhythmogenesis[J].FASEB J,2013,27:1460-1467.
[16]	IACONETTI C,POLIMENI A,SORRENTINO S,et al.Inhibition of miR-92aincreases endothelial proliferation and migration in vitro as well as reduces neointimal proliferation in vivo after vascular injury[J].Basic Res Cardiol,2012,107:1-14.
[17]	HINKEL R,PENZKOFER D,Z?HLKE S,et al.Inhibition of microRNA-92aprotects against ischemia/reperfusion injury in a large-animal model[J].Circulation,2013,128:1066-1075.
[18]	PIN A L,HOULE F,GUILLONNEAU M,et al.miR-20arepresses endothelial cell migration by targeting MKK3 and inhibiting p38 MAP kinase activation in response to VEGF[J].Angiogenesis,2012,15:593-608.
[19]	SUÁREZ Y,FERN?NDEZ-HERNANDO C,YU J,et al.Dicer-dependent endothelial microRNAs are necessary for postnatal angiogenesis[J].Proc Natl Acad Sci USA,2008,105:14082-14087.
[20]	SEMO J,SHARIR R,AFEK A,et al.The 106b-25 microRNA cluster is essential for neovascularization after hindlimb ischaemia in mice[J].Eur Heart J,2014,35:3212-3223.
[21]	ICLI B,WARA A K,MOSLEHI J,et al.MicroRNA-26aregulates pathological and physiological angiogenesis by targeting BMP/SMAD1 signaling[J].Circ Res,2013,113:1231-1241.
[22]	SPINETTI G,FORTUNATO O,CAPORALI A,et al.MicroRNA-15aand microRNA-16impair human circulating proangiogenic cell functions and are increased in the proangiogenic cells and serum of patients with critical limb ischemia[J].Circ Res,2013,112:335-346.
[23]	HU S,HUANG M,LI Z,et al.MicroRNA?210as a novel therapy for treatment of ischemic heart disease[J].Circulation,2010,122:S124-S131.
[24]	MATSA E,SALLAM K,WU J C.Cardiac stem cell biology:glimpse of the past,present,and future[J].Circ Res,2014,114:21-27.
[25]	DIMMELER S,DING S,RANDO T A,et al.Translational strategies and challenges in regenerative medicine[J].Nat Med,2014,20:814-821.
[26]	JANSEN F,YANG X,HOELSCHER M,et al.Endothelial microparticle-mediated transfer of microRNA-126promotes vascular endothelial cell repair via SPRED1 and is abrogated in glucose-damaged endothelial microparticles[J].Circulation,2013,128:2026-2038.
[27]	HUANG F,ZHU X,HU X Q,et al.Mesenchymal stem cells modified with miR-126release angiogenic factors and activate Notch ligand Delta-like-4,enhancing ischemic angiogenesis and cell survival[J].Int J Mol Med,2013,31:484-492.
[28]	LIU J,VAN MIL A,VRIJSEN K,et al.MicroRNA-155prevents necrotic cell death in human cardiomyocyte progenitorcells via targeting RIP1[J].J Cell Mol Med,2011,15:1474-1482.
[29]	XU Q,SEEGER F H,CASTILLO J,et al.MicroRNA-34acontributes to the impaired function of bone marrow-derived mononuclear cells from patients with cardiovascular disease[J].J Am Coll Cardiol,2012,59:2107-2117.
[30]	HU S,HUANG M,NGUYEN P K,et al.Novel MicroRNA prosurvival cocktail for improving engraftment and function of cardiac progenitor cell transplantation[J].Circulation,2011,124:S27-S34.
[31]	JAYAWARDENA T M,EGEMNAZAROV B,FINCH E A,et al.MicroRNA-mediated in vitro and in vivo direct reprogramming of cardiac fibroblasts to cardiomyocytes[J].Circ Res,2012,110:1465-1473.
[32]	NAM Y J,SONG K,LUO X,et al.Reprogramming of human fibroblasts toward a cardiac fate[J].Proc Natl Acad Sci USA,2013,110:5588-5593.
[33]	JAYAWARDENA T M,FINCH E A,ZHANG L,et al.MicroRNA induced cardiac reprogramming in vivo:evidence for mature cardiac myocaytes and improved cardiac function[J].Circ Res,2015,116:418-424.
[34]	BOON R A,VICKERS K C.Intercellular transport of microRNAs[J].Arterioscler Thromb Vasc Biol,2013,33:186-192.
[35]	MOCHARLA P,BRIAND S,GIANNOTTI G,et al.AngiomiR-126expression and secretion from circulating CD34+ and CD14+ PBMCs:role for proangiogenic effects and alterations in type 2diabetics[J].Blood,2013,121:226-236.
[36]	BARILE L,LIONETTI V,CERVIO E,et al.Extracellular vesicles from human cardiac progenitor cells inhibit cardiomyocyte apoptosis and improve cardiac function after myocardial infarction[J].Cardiovasc Res,2014,103:530-541.
[37]	ONG S G,LEE W H,HUANG M,et al.Cross talk of combined gene and cell therapy in ischemic heart disease:role of exosomal microRNA transfer[J].Circulation,2014,130:S60-S69.
[38]	CHENG H S,SIVACHANDRAN N,LAU A,et al.MicroRNA-146represses endothelial activation by inhibiting proinflammatory pathways[J].EMBO Mol Med,2013,5:949-966.
[39]	BELLERA N,BARBA I,RODRIGUEZ-SINOVAS A,et al.Single intracoronary injection of encapsulated antagomiR-92a promotes angiogenesis and prevents adverse infarct remodeling[J].J Am Heart Assoc,2014,3:e000946.