2025年5月25日 周日
Home > Archive>Volume 29, Issue 11, 2021 >1007-1012
PDF HTML XML Export Cite reminder
Research progress of miR-206 and cardiovascular disease
Author:
Affiliation:

1.The Cardiovascular Medicine Department of First Clinical Medical College, Shanxi Medical University;2.Key laboratory of Cellular Physiology of Shanxi Medical University, Ministry of Education;3.The Cardiovascular Medicine Department of the First Hospital of Shanxi Medical University, Taiyuan, Shanxi 030001, China)

  • Article
    • | |
  • Metrics
    • |
  • Reference [53]
    • | | | |
  • Comments
    Abstract:

    MicroRNAs (miRNAs), a large class of short non-coding RNAs, can directly bind to the 3′ untranslated region of target genes, thus affecting gene expression and playing a key role in cardiovascular diseases. Among them, miRNA-206 (miR-206) is a key regulator of heart development and physiological activities, and can not only be used as a marker molecule for diagnosis, but also as a targeted action point for disease treatment. This paper reviews the basic functions of miR-206 in regulating cardiomyocytes, endothelial cells, smooth muscle cells, autonomic nerve cells and other cells, as well as the specific roles and mechanisms of miR-206 in the occurrence and development of coronary artery disease, myocardial infarction, heart failure, arrhythmia, pulmonary hypertension and other diseases.

    Reference
    [1] FABIAN M R, SONENBERG N.The mechanics of miRNA-mediated gene silencing:a look under the hood of miRISC.Nat Struct Mol Biol, 2,9(6):586-593.
    [2] FICHTLSCHERER S, ZEIHER A M, DIMMELER S.Circulating microRNAs:biomarkers or mediators of cardiovascular diseases?.Arterioscler Thromb Vasc Biol, 1,1(11):2383-2390.
    [3] BOETTGER T, WST S, NOLTE H, et al.The miR-206/133b cluster is dispensable for development, survival and regeneration of skeletal muscle.Skelet Muscle, 4,4(1):23.
    [4] 康治理, 武振方, 刘晓伟, 等.基于生物信息学分析的hsa-miR-206靶基因预测.东南国防医药, 0,2(2):118-123.
    [5] RUSANOVA I, FERNNDEZ-MARTNEZ J, FERNNDEZ-ORTIZ M, et al.Involvement of plasma miRNAs, muscle miRNAs and mitochondrial miRNAs in the pathophysiology of frailty.Exp Gerontol, 9,4:110637.
    [6] NOVK J, VINKLREK J, BIENERTOV-VASˇKU J, et al.MicroRNAs involved in skeletal muscle development and their roles in rhabdomyosarcoma pathogenesis.Pediatr Blood Cancer, 3,0(11):1739-1746.
    [7] WANG Y, GUO T, LIU Q, et al.CircRAD18 accelerates the progression of acute myeloid leukemia by modulation of miR-206/PRKACB axis.Cancer Manag Res, 0,2:10887-10896.
    [8] ZHANG H, WANG J, REN T, et al.Bone marrow mesenchymal stem cell-derived exosomal miR-206 inhibits osteosarcoma progression by targeting TRA2B.Cancer Lett, 0,0:54-65.
    [9] ZHENG Y, YANG X, WANG C, et al.HDAC6, modulated by miR-206, promotes endometrial cancer progression through the PTEN/Akt/mTOR pathway.Sci Rep, 0,0(1):3576.
    [10] ZEHTABIAN S H, ALIBAKHSHI R, SEYEDENA S Y, et al.Relationship between microRNA-206 plasma levels with the severity of coronary artery conflicts in patients with coronary artery disease.Bratisl Lek Listy, 9,0(8):581-585.
    [11] 郑莹, 马艳玲, 谷秀莲, 等.miR-206对血管内皮细胞增殖的影响及其机制.中国动脉硬化杂志, 9,7(6):475-480.
    [12] WANG M, JI Y, CAI S, et al.miR-206 suppresses the progression of coronary artery disease by modulating vascular endothelial growth factor (VEGF) expression.Med Sci Monit, 6,2:5011-5020.
    [13] HRISTOV M, ZERNECKE A, LIEHN E A, et al.Regulation of endothelial progenitor cell homing after arterial injury.Thromb Haemost, 7,8(2):274-277.
    [14] ACKAH E, YU J, ZOELLNER S, et al.Akt1/protein kinase Balpha is critical for ischemic and VEGF-mediated angiogenesis.J Clin Invest, 5,5(8):2119-2127.
    [15] TANG Y, ZHANG Y, CHEN Y, et al.Role of the microRNA, miR-206, and its target PIK3C2α in endothelial progenitor cell function-potential Link with coronary artery disease.FEBS J, 5,2(19):3758-3772.
    [16] HAN X, LIU L, NIU J, et al.Serum VEGF predicts worse clinical outcome of patients with coronary heart disease after percutaneous coronary intervention therapy.Med Sci Monit, 5,1:3247-3251.
    [17] DORAN A C, MELLER N, MCNAMARA C A.Role of smooth muscle cells in the initiation and early progression of atherosclerosis.Arterioscler Thromb Vasc Biol, 8,8(5):812-819.
    [18] BOT P T, GRUNDMANN S, GOUMANS M J, et al.Forkhead box protein P1 as a downstream target of transforming growth factor-β induces collagen synthesis and correlates with a more stable plaque phenotype.Atherosclerosis, 1,8(1):33-43.
    [19] XING T, DU L, ZHUANG X, et al.Upregulation of microRNA-206 induces apoptosis of vascular smooth muscle cells and decreases risk of atherosclerosis through modulating FOXP1.Exp Ther Med, 7,4(5):4097-4103.
    [20] LI H, XIANG Y, FAN L J, et al.Myocardin inhibited the gap protein connexin 43 via promoted miR-206 to regulate vascular smooth muscle cell phenotypic Switch.Gene, 7,6:22-30.
    [21] LI P, ZHU N, YI B, et al.MicroRNA-663 regulates human vascular smooth muscle cell phenotypic Switch and vascular neointimal formation.Circ Res, 3,3(10):1117-1127.
    [22] SUN H, CAI S, ZHANG M, et al.MicroRNA-206 regulates vascular smooth muscle cell phenotypic Switch and vascular neointimal formation.Cell Biol Int, 7,1(7):739-748.
    [23] CHEN J, HSIEH A F, DHARMARAJAN K, et al.National trends in heart failure hospitalization after acute myocardial infarction for Medicare beneficiaries:1998-2010.Circulation, 3,8(24):2577-2584.
    [24] TOWER J.Programmed cell death in aging.Ageing Res Rev, 5,3(Pt A):90-100.
    [25] SHAN Z X, LIN Q X, FU Y H, et al.Upregulated expression of miR-1/miR-206 in a rat model of myocardial infarction.Biochem Biophys Res Commun, 9,1(4):597-601.
    [26] SHAN Z X, LIN Q X, DENG C Y, et al.miR-1/miR-206 regulate Hsp60 expression contributing to glucose-mediated apoptosis in cardiomyocytes.FEBS Lett, 0,4(16):3592-3600.
    [27] 江哿, 何清, 张卉, 等.miR-206-3p通过LXRα调控糖尿病心肌病心肌细胞凋亡的研究.心血管康复医学杂志, 0,9(4):418-424.
    [28] DENG L, HONG T, LIN J, et al.Histamine deficiency exacerbates myocardial injury in acute myocardial infarction through impaired macrophage infiltration and increased cardiomyocyte apoptosis.Sci Rep, 5,5:13131.
    [29] DING S, ABUDUPATAER M, ZHOU Z, et al.Histamine deficiency aggravates cardiac injury through miR-206/216b-Atg13 axis-mediated autophagic-dependant apoptosis.Cell Death Dis, 8,9(6):694.
    [30] NGUYEN T D, SCHWARZER M, SCHREPPER A, et al.Increased protein tyrosine phosphatase 1B (PTP1B) activity and cardiac insulin resistance precede mitochondrial and contractile dysfunction in Pressure-Overloaded hearts.J Am Heart Assoc, 8,7(13):e008865.
    [31] YAN Y, DANG H, ZHANG X, et al.The protective role of miR-206 in regulating cardiomyocytes apoptosis induced by ischemic injury by targeting PTP1B.Biosci Rep, 0,0(1):BSR20191000.
    [32] ZHAI C, QIAN Q, TANG G, et al.MicroRNA-206 protects against myocardial Ischaemia-Reperfusion injury in rats by targeting Gadd45β.Mol Cells, 7,0(12):916-924.
    [33] YANG Y, DEL RE D P, NAKANO N, et al.miR-206 mediates YAP-Induced cardiac hypertrophy and survival.Circ Res, 5,7(10):891-904.
    [34] 邴艳萍, 宋璇, 姜楠, 等.lncRNA NEAT1调控miR-206对缺氧复氧大鼠心肌细胞氧化应激损伤和凋亡的影响.中国动脉硬化杂志, 0,8(12):1034-1041.
    [35] TCHAO J, KIM J J, LIN B, et al.Engineered human muscle tissue from skeletal muscle derived stem cells and induced pluripotent stem cell derived cardiac cells.Int J Tissue Eng, 2013:198762.
    [36] TCHAO J, HAN L, LIN B, et al.Combined biophysical and soluble factor modulation induces cardiomyocyte differentiation from human muscle derived stem cells.Sci Rep, 4,4:6614.
    [37] GUTSTEIN D, MORLEY G E, TAMADDON H, et al.Conduction slowing and sudden arrhythmic death in mice with cardiac-restricted inactivation of connexin43.Circ Res, 1,8(3):333-339.
    [38] WESTENDORP B, MAJOR J L, NADER M, et al.The E2F6 repressor activates gene expression in myocardium resulting in dilated cardiomyopathy.FASEB J, 2,6(6):2569-2579.
    [39] DING H S, YANG J.High mobility group box-1 and cardiovascular diseases.Saudi Med J, 0,1(5):486-489.
    [40] LIMANA F, ESPOSITO G, D'ARCANGELO D, et al.HMGB1 attenuates cardiac remodelling in the failing heart via enhanced cardiac regeneration and miR-206-mediated inhibition of TIMP-3.PLoS One, 1,6(6):e19845.
    [41] ZHU X J, HUA Y, JIANG J, et al.Neuronal nitric oxide synthase-derived nitric oxide inhibits neurogenesis in the adult dentate gyrus by down-regulating cyclic AMP response element binding protein phosphorylation.Neuroscience, 6,1(2):827-836.
    [42] WEI J, ZHANG Y, LI Z, et al.GCH1 attenuates cardiac autonomic nervous remodeling in canines with atrial-tachypacing via tetrahydrobiopterin pathway regulated by microRNA-206.Pacing Clin Electrophysiol, 8,1(5):459-471.
    [43] GOETTE A, BUKOWSKA A, LILLIG C H, et al.Oxidative stress and microcirculatory flow abnormalities in the ventricles during atrial fibrillation.Front Physiol, 2,3:236.
    [44] GAO J, ZHONG M K, FAN Z D, et al.SOD1 overexpression in paraventricular nucleus improves post-infarct myocardial remodeling and ventricular function.Pflugers Arch, 2,3(2):297-307.
    [45] ZHANG Y, ZHENG S, GENG Y, et al.MicroRNA profiling of atrial fibrillation in canines:miR-206 modulates intrinsic cardiac autonomic nerve remodeling by regulating SOD1.PLoS One, 5,0(3):e0122674.
    [46] JIN Y, ZHOU T Y, CAO J N, et al.MicroRNA-206 downregulates connexin43 in cardiomyocytes to induce cardiac arrhythmias in a transgenic mouse model.Heart Lung Circ, 9,8(11):1755-1761.
    [47] JIN Y, ZHOU T, FENG Q, et al.Inhibition of MicroRNA-206 ameliorates Ischemia-Reperfusion arrhythmia in a mouse model by targeting connexin43.J Cardiovasc Transl Res, 0,3(4):584-592.
    [48] JIN P, GU W, LAI Y, et al.The circulating MicroRNA-206 level predicts the severity of pulmonary hypertension in patients with left heart diseases.Cell Physiol Biochem, 7,1(6):2150-2160.
    [49] JALALI S, RAMANATHAN G K, PARTHASARATHY P T, et al.miR-206 regulates pulmonary artery smooth muscle cell proliferation and differentiation.PLoS One, 2,7(10):e46808.
    [50] YUE J, GUAN J, WANG X, et al.MicroRNA-206 is involved in hypoxia-induced pulmonary hypertension through targeting of the HIF-1α/Fhl-1 pathway.Lab Invest, 3,3(7):748-759.
    [51] 白延平, 李海军, 刘智娜.miR-206在大鼠肺动脉高压模型中的表达和意义.心脏杂志, 9,1(6):654-659.
    [52] LV Y, TANG L L, WEI J K, et al.Decreased Kv1.5 expression in intrauterine growth retardation rats with exaggerated pulmonary hypertension.Am J Physiol Lung Cell Mol Physiol, 3,5(11):L856-L865.
    [53] LV Y, FU L, ZHANG Z, et al.Increased expression of microRNA-206 inhibits Potassium Voltage-Gated Channel subfamily a member 5 in pulmonary arterial smooth muscle cells and is related to exaggerated pulmonary artery hypertension following intrauterine growth retardation in rats.J Am Heart Assoc, 9,8(2):e010456.
    Related
    Cited by
    Comments
    Comments
    分享到微博
    Submit
Get Citation

WANG Haoyue, TIAN Jing, HAN Qinghua. Research progress of miR-206 and cardiovascular disease[J]. Editorial Office of Chinese Journal of Arteriosclerosis,2021,29(11):1007-1012.

Copy
Share
Article Metrics
  • Abstract:489
  • PDF: 708
  • HTML: 0
  • Cited by: 0
History
  • Received:January 08,2021
  • Revised:July 07,2021
  • Online: November 18,2021
Article QR Code

You are the 48827 visitor

Post Code：421001 Fax：0734-8160523

Phone：0734-8160765 E-mail：dmzzbjb@163.net

Editorial Office of Chinese Journal of Arteriosclerosis ® 2025