[1]李光召 王艳 石蓓 *.MicroRNAs与心肌重构的研究新进展[J].心血管病学进展,2020,(2):196-200.[doi:10.16806/j.cnki.issn.1004-3934.2020.02.025]
　LI Guangzhao,WANG Yan,SHI Bei.MicroRNAsNew Target for Ventricular Remodeling Treatment[J].Advances in Cardiovascular Diseases,2020,(2):196-200.[doi:10.16806/j.cnki.issn.1004-3934.2020.02.025]
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MicroRNAs与心肌重构的研究新进展()
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《心血管病学进展》[ISSN:51-1187/R/CN:1004-3934]

卷:
期数:
2020年2期
页码:
196-200
栏目:
综述
出版日期:
2020-02-25

文章信息/Info

Title:
MicroRNAsNew Target for Ventricular Remodeling Treatment
作者:
李光召 王艳 2 石蓓 3*
(1.遵义医科大学心血管内科,贵州 遵义 563000;2.遵义医科大学第一附属医院心血管内科,贵州 遵义 563000;3. 遵义医科大学第一附属医院心血管内科,贵州 遵义 563000)
Author(s):
LI Guangzhao1;  WANG Yan2;  SHI Bei3
(Department of Cardiology Laboratory of Zunyi Medical University, Zunyi 563000, Guizhou, China)
关键词:
MicroRNAs; 心室重构; 心力衰竭
Keywords:
MicroRNAs;  Ventricular remodeling; Heart failure
DOI:
10.16806/j.cnki.issn.1004-3934.2020.02.025
摘要:
随着医疗水平的提高，特别是冠心病介入治疗水平的提高，因心肌梗死引起的死亡率正逐年降低，但是因心肌梗死后的心室重构导致的心力衰竭发生率正逐年增加。目前临床上针对心室重构的治疗仍缺乏有效手段，因心力衰竭导致的死亡正逐年增加。越来越多的研究表明microRNAs在多种心脏病中发挥重要的作用，并且与心室重构有着密切的联系。现就microRNAs在心室重构中的作用展开综述，探讨microRNAs在其病理生理过程中的功能和作用及针对心室重构治疗的新方法。
Abstract:
Along with the improvement of medical level, especially the treatment level improvement of percutaneous coronary intervention, the death rate caused by myocardial infarction is reducing year by year. Whereas, the incidence rate of heart failure due to ventricular remodeling for myocardial infarction is increasing year by year. It still lacks efficient methods in clinical applications for the treatment of ventricular remodeling for myocardial infarction, the death caused by heart failure is increasing year by year. More and more researches show that microRNAs play important roles in many heart diseases and has close connection with ventricular remodeling. Hence, this article summarizes the actions of microRNAs in ventricular remodeling, and discusses the function and effect of microRNAs in the pathophysiology progress, and the new method for ventricular remodeling treatment

参考文献/References:

[1] Romaine SPR, Tomaszewski M, Condorelli G, et al. MicroRNAs in cardiovascular disease: an introduction for clinicians[J]. Heart, 2015,101(12):921-928.

[2] 张倩,宋林声,赵新湘. MicroRNA 21与冠心病相关性的研究进展[J]. 心血管病学进展, 2018,39(4):598-601.

[3] Wang J, Liew O, Richards A, et al. Overview of microRNAs in cardiac hypertrophy, fibrosis, and apoptosis[J]. Int J Mol Sci, 2016,17(5):749.

[4] Tham YK, Bernardo BC, Ooi JYY, et al. Pathophysiology of cardiac hypertrophy and heart failure: signaling pathways and novel therapeutic targets[J]. Arch Toxicol, 2015,89(9):1401-1438.

[5] Demkes CJ, van Rooij E. MicroRNA-146a as a regulator of cardiac energy metabolism[J]. Circulation, 2017,136(8):762-764.

[6] Chen C, Ponnusamy M, Liu C, et al. MicroRNA as a therapeutic target in cardiac remodeling[J]. BioMed Res Int, 2017,2017:1-25.

[7] Guo H, Ingolia NT, Weissman JS, et al. Mammalian microRNAs predominantly act to decrease target mRNA levels[J]. Nature, 2010,466(7308):835-840.

[8] Das S, Kohr M, Dunkerly Eyring B, et al. Divergent effects of miR‐181 family members on myocardial function through protective cytosolic and detrimental mitochondrial microRNA targets[J]. J Am Heart Assoc, 2017,6(3).?pii: e004694.

[9] Elizabeth H, Leptidis S, Dirkx E, et al. The hypoxia-inducible microRNA cluster miR-199a?214 targets myocardial PPARδ and impairs mitochondrial fatty acid oxidation[J]. Cell Metabolism, 2013,18(3):341-354.

[10] Osama Abo A, Said K, Saleh AN. MicroRNAs 33, 122, and 208: a potential novel targets in the treatment of obesity, diabetes, and heart-related diseases[J]. J Physiol Biochem, 2017,73(2):307-314.

[11] Weitzel RP, Lesniewski ML, Haviernik P, et al. microRNA 184 regulates expression of NFAT1 in umbilical cord blood CD4+ T cells[J]. Blood, 2009,113(26):6648-6657.

[12] Li W, Kong L, Li J, et al. MiR-568 inhibits the activation and function of CD4+ T cells and Treg cells by targeting NFAT5[J]. International Immunology, 2014,26(5):269-281.

[13] Kang K, Peng X, Zhang X, et al. MicroRNA-124 suppresses the transactivation of nuclear factor of activated T cells by targeting multiple genes and inhibits the proliferation of pulmonary artery smooth muscle cells[J]. J Biol Chem, 2013,288(35):25414-25427.

[14] Zeng Y, Wang Y, Wu Z, et al. miR-9 enhances the transactivation of nuclear factor of activated T cells by targeting KPNB1 and DYRK1B[J]. Am J Physiol Cell Physiol, 2015,308(9):C720-C728.

[15] da Costa Martins PA, Salic K, Gladka MM, et al. MicroRNA-199b targets the nuclear kinase Dyrk1a in an auto-amplification loop promoting calcineurin/NFAT signalling[J]. Nat Cell Biol, 2010,12(12):1220-1227.

[16] Song DW, Ryu JY, Kim JO, et al. ThemiR-19a/b family positively regulates cardiomyocyte hypertrophy by targeting atrogin-1 and MuRF-1[J]. Biochem J, 2014,457(1):151-162.

[17] Ge Y, Pan S, Guan D, et al. MicroRNA-350 induces pathological heart hypertrophy by repressing both p38 and JNK pathways[J]. Biochim Biophys Acta, 2013,1832(1):1-10.

[18] Ucar A, Gupta SK, Fiedler J, et al. The miRNA-212/132 family regulates both cardiac hypertrophy and cardiomyocyte autophagy[J]. Nature Communications, 2012,3(1):1078.

[19] Sun X, Zhang C. MicroRNA-96 promotes myocardial hypertrophy by targeting mTOR[J]. Int J Clin Exp Pathol, 2015,8(11):14500-14506.

[20] Li Z, Song Y, Liu L, et al. MiR-199a impairs autophagy and induces cardiac hypertrophy through mTOR activation[J]. Cell Death Differ, 2017,24(7):1205-1213.

[21] Huang J, Sun W, Huang H, et al. MiR-34a modulates angiotensin Ⅱ-induced myocardial hypertrophy by direct inhibition of ATG9A expression and autophagic activity[J]. PLoS ONE, 2014,9(4):e94382.

[22] Pan W, Zhong Y, Cheng C, et al. MiR-30-regulated autophagy mediates angiotensin Ⅱ-induced myocardial hypertrophy[J]. PLoS ONE, 2013,8(1):e53950.

[23] Xu F, Kang Y, Zhang H, et al. Akt1-mediated regulation of macrophage polarization in a murine model of staphylococcus aureus pulmonary infection[J]. J Infect Dis, 2013,208(3):528-538.

[24] Zhang Y, Zhang M, Li X, et al. Silencing microRNA-155 attenuates cardiac injury and dysfunction in viral myocarditis via promotion of M2 phenotype polarization of macrophages[J]. Sci Rep, 2016,6(1):22613.

[25] Wu X, Dai Y, Yang Y, et al. Emerging role of microRNAs in regulating macrophage activation and polarization in immune response and inflammation[J]. Immunology, 2016,148(3):237-248.

[26] Liu Y, Wang H, Wang X, et al. MiR-29b inhibits ventricular remodeling by activating notch signaling pathway in the rat myocardial infarction model[J]. Heart Surg Forum, 2019,22(1):E19-E23.

[27] Thum T, Gross C, Fiedler J, et al. MicroRNA-21 contributes to myocardial disease by stimulating MAP kinase signalling in fibroblasts[J]. Nature, 2008,456(7224):980-984.

[28] Tijsen A J, van der Made I, van den Hoogenhof MM, et al. The microRNA-15 family inhibits the TGFβ-pathway in the heart[J]. Cardiovasc Res, 2014,104(1):61-71.

[29] Sassi Y, Avramopoulos P, Ramanujam D, et al. Cardiac myocyte miR-29 promotes pathological remodeling of the heart by activating Wnt signaling[J]. Nat Commun, 2017,8(1):1614.

[30] Kim SW, Ramasamy K, Bouamar H, et al. MicroRNAs miR-125a and miR-125b constitutively activate the NF-κB pathway by targeting the tumor necrosis factor alpha-induced protein 3 (TNFAIP3, A20)[J]. Proc Natl Acad Sci U S A , 2012,109(20):7865-7870.

[31] Kannambath S. Micro-RNA feedback loops modulating the calcineurin/NFAT signaling pathway[J]. Noncoding RNA, 2016,2(2).pii:E3.

[32] Dirkx E, Gladka MM, Philippen LE, et al. Nfat and miR-25 cooperate to reactivate the transcription factor Hand2 in heart failure[J]. Nat Cell Biol, 2013,15(11):1282-1293.

[33] Gao M, Wang X, Zhang X, et al. Attenuation of cardiac dysfunction in polymicrobial sepsis by microRNA-146a is mediated via targeting of IRAK1 and TRAF6 expression[J].J Immunol, 2015,195(2):672-682.

[34] Davis J, Molkentin JD. Myofibroblasts:trust your heart and let fate decide[J]. J Mol Cell Cardiol, 2014,70:9-18.

[35] Seok HY, Chen J, Kataoka M, et al. Loss of microRNA-155 protects the heart from pathological cardiac hypertrophy[J]. Circ Res, 2014,114(10):1585-1595.

[36] Roncarati R, Viviani Anselmi C, Losi MA, et al. Circulating miR-29a, among other up-regulated microRNAs, is the only biomarker for both hypertrophy and fibrosis in patients with hypertrophic cardiomyopathy[J]. J Am Coll Cardiol, 2014,63(9):920-927.

[37] Derda AA, Thum S, Lorenzen JM, et al. Blood-based microRNA signatures differentiate various forms of cardiac hypertrophy[J]. Int J Cardiol, 2015,196:115-122.

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更新日期/Last Update: 2020-04-14