SYSTEMS INTERACTION microRNAs IN PATHOGENESIS OF CARDIOVASCULAR DISEASES

Authors

DOI:

https://doi.org/10.11603/mie.1996-1960.2019.3.10428

Keywords:

systems medicine, microRNAs (miRNAs), cardial hyperthrophy, fibrosis, apoptosis, cardiovascular disease, network, regulation.

Abstract

Background. A review - analytical article is devoted to the analysis of the role of microRNAs (miRNAs) in modulating gene expression in biological events, primarily in cardiovascular diseases. Separate microRNAs are presented that have a systemic regulatory effect on the expression of target genes of processes such as myocardial hypertension, fibrosis, and apoptosis.

Purpose. The purpose of this review is to analyze the literature data on the regulatory effects of microRNAs in heart remodeling, in particular with myocardial hypertrophy, fibro-formation and apoptosis.

Results. Materials and methods. A group of miRNAs is analyzed, which may be of particular importance in the ontogenesis of cardiovascular diseases (CVD), since they modulate the expression of genes from target clusters, sites of many pathological cardiovascular reactions, the review illustrates the involvement of miRNAs in the network interaction of intracellular signaling pathways and positions important regulatory microRNA cooperation in CVD. It is postulated that the accumulated data on the role of miRNAs in the pathogenesis of diseases, primarily in the pathogenesis of cardiovascular diseases, are the basis for subsequent innovative solutions in the development of diagnostic methods and systemic therapy based on the use of post-translational regulators.

Conclusion. Circulating miRNAs can be proposed as promising diagnostic and prognostic biomarkers of CVDs, such as myocardial infarction, atherosclerosis, coronary heart disease, heart failure, etc.

References

Berezin, A. E., Kremser, A. A. (2014). Potentsyalnaia dyahnostycheskaia y prohnostycheskaia rol mikroRNK kak byolohycheskykh markerov voznyknovenyia y prohressyrovanyia serdechnoi nedostatochnosty [Potential diagnostic and prognostic role of miRNAs as biological markers of the occurrence and progression of heart failure]. Sertse i sudyny (Heart and blood vessels), 3, 93-101. [In Russian].

Zalessky, V. N., Filchenkov, A. A., Gavrilenko, T. I. (2002). Apoptoz pry yshemyy y reperfuzyy myokarda [Apoptosis in myocardial ischemia and reperfusion]. Likarska sprava (Medical business), 1, 8-15. [In Russian].

Kovalenko, V. N., Kuchtenko, Ye. B., Mkhitaryan, L. S. (2014). Rol odynochnikh nukleotydnikh polymorfyzmov v mikroRNK v patoheneze zabolevanyi serdechno-sosudystoi systemi [The role of single nucleotide polymorphisms and miRNAs in the pathogenesis of diseases of the cardiovascular system]. Zhurnal NAMN Ukrainyi (Journal of NAMS of Ukraine), 20 (1), 62-73. [In Russian].

Lutay, M. I., Lysenko, A. F., Telegeev, G. D. et al. (2012). Znachenie mikroRNK pri serdechno-sosudistoy patologii [The value of microRNA in cardiovascular disease]. Ukrayinskiy kardIologIchniy zhurnal (Ukrainian Cardiology Journal), 6, 17-24. [In Russian].

Romashov, G. A. (2018). Epigeneticheskaya regulyatsiya ekspressii genov mikroRNK pri ateroskleroze sonnyih arteriy u cheloveka: dis. ... magistra biologii: 06.04.01 [Epigenetic regulation of miRNA gene expression in carotid arteriosclerosis in humans: dis. ... Master of Biology: 06.04.01]. Tomsk. [In Russian].

Romakina, V. V., Zhirov, N. V., Nasonova, S. N. et al. (2008). MikroRNK kak biomarkeryi serdechno-sosudistyih zabolevaniy [MicroRNA as biomarkers of cardiovascular diseases]. Kardiologiya (Cardiology), 58 (1), 66-71. [In Russian].

Shvangiradze, T. A., Bondarenko, I. Z., Troshina, E. A. et al. (2016). MikroRNK v diagnostike serdechno-sosudistyih zabolevaniy, assotsiirovannyih s saharnyim diabetom 2-go tipa i ozhireniem [MicroRNA in the diagnosis of cardiovascular diseases associated with type 2 diabetes and obesity]. Terapevticheskiy arhiv (Therapeutic Archive), 10, 87-92. [In Russian]. DOI: https://doi.org/10.17116/terarkh201688687-92

Adam, O., Lohfelm, B., Thum, T. et al. (2012). Role of miR-21 in the pathogenesis of atrial fibrosis. Basic Res. Cardiol., 107 (5), 278. DOI: https://doi.org/10.1007/s00395-012-0278-0

Bartel, D. P. (2004). Review of microRNAS: genomics, biogenesis, mechanisms and function. Cell, 116 (2), 281-297.

Bayonmi, A. S., Aonuma, T., Teoh, J. P. et al. (2018). Circular noncoding RNAS as a potential therapeutic and circulating biomarkers for cardiovascular diseases. Acta Pharmacol. Sin., 38 (7), 1100-1109. DOI: https://doi.org/10.1038/aps.2017.196

Callis, T. E., Pandya, K., Seok, H. Y. et al. (2009). MicroRNA-208a is a regulator of cardiac hypertrophy and conduction in nice. J. Clin. Invest., 119 (9), 2722786.

Care, A., Catalucci, D., Felicetti, F. et al. (2007). MicroRNA-133 controls cardiac hyperthrophy. Nat. Med., 13 (5), 613-618. DOI: https://doi.org/10.1038/nm1582

Castoldi, G., Di Gioia, C. R., Bombardi, C. et al. (2012). MiR-133a regulates collagen 1A1: potential role of miR-133a in myocardial fibrosis in angiotensin II dependent hypertension. J. Cell Physiol., 227 (2), 850-856. DOI: https://doi.org/10.1002/jcp.22939

Condorelli, G., Latronico, M. V., Cavarreta, E. (2014). MicroRNAS in cardiovascular diseases: current knowledge and the road ahead. J. Am. Coll. Cardiol., 63, 2177-2187. DOI: https://doi.org/10.1016/j.jacc.2014.01.050

Da Costa Martins, P. A., Salic, K., Gladka, M. M. et al. (2010). MicroRNA-199b target the nuclear kinase Dyrk1a in an auto-amplification loop promoting calcineurin/NFAT signaling. Nat. Cell Biol., 12 (12), 1220-1227. DOI: https://doi.org/10.1038/ncb2126

Duan, Y., Zhon, B., Su, H. et al. (2013). MiR-150 regulates high glucose induced cardiomyocyte hypertrophy by targeting the transcriptional co-activator p300. Exp. Cell Res., 319 (3), 173-184. DOI: https://doi.org/10.1016/j.yexcr.2012.11.015

Duan, Q., Chen, C., Yang, L. et al. (2015). MicroRNA regulation of unfolded protein response transcription factor XBP1 in the progression of cardiac hypertrophy and heart failure in vivo. J. Transl. Med., 13, 363. DOI: https://doi.org/10.1186/s12967-015-0725-4

Duisters, R. F., Tijsen, A. J., Schroen, B. et al. (2009). MiR-133 and miR-30 regulate connective tissue growth factor: implications for a role of MicroRNAS in myocardial matrix remodeling. Circ. Res., 104 (2), 170-178. DOI: https://doi.org/10.1161/CIRCRESAHA.108.182535

Eisenberg, I., Eran, A., Nishino, J. et al. (2007). Distinctive patterns of microRNA expression in primary muscular disorders. Proc. Natl. Acad. Sci., 104 (43), 17016-17021. DOI: https://doi.org/10.1073/pnas.0708115104

Fang, J., Song, X. W., Tian, J. et al. (2012). Over expression of microRNA-378 attenuates ischemia-induced apoptosis by inhibiting caspase-3 expression in cardiac myocytes. Apoptosis, 17 (4), 410-423. DOI: https://doi.org/10.1007/s10495-011-0683-0

Gallurzi, L., Bravo-SanPedro, J. M., Vital, I. et al. (2015). Essential versus accessory aspect of cell death. Cell Death Differ., 22 (1), 58-73.

Ganesan, J., Ramanujan, D., Sassi, Y. et al. (2013). MiR-378 controls cardiac hyperthrophy by combined repression of mitogen-activated protein kinase pathways. Circulation, 127 (21), 2097-2106. DOI: https://doi.org/10.1161/CIRCULATIONAHA.112.000882

Greenland, H., Alpert, J. S., Beller, G. A. et al. (2010). ACCF/AHA guideline for assessment of cardiovascular risk in asymptomatic adults: a report of the American College of Cardiology Foundation. Circulation, 122 (25), e584-636.

Han, M., Yang, Z., Sayed, D. et al. (2012). GATA4 expression is primarily regulated via a miR-26b dependent post-transcriptional mechanism during cardial hyperthrophy. Cardiovasc. Res., 93 (4), 645-654. DOI: https://doi.org/10.1093/cvr/cvs001

He, W., Huang, H., Xie, Q. et al. (2016). MiR-155 Knockout in fibroblast improves cardiac remodeling by targeting tumor protein p53 inducible nuclear protein 1. J. Cardiovasc. Pharmacol., Ther., 21 (4), 423-435. DOI: https://doi.org/10.1177/1074248415616188

Hong, S., Lee, J., Seo, H. H. et al. (2015). Na (+) - Ca (2+) exchanger targeting miR-132prevents apoptosis of cardiomyocytes under hypoxic condition by suppressing Ca (2+) overload. Biochem. Biophys. Res. Commun., 460 (4), 931-937. DOI: https://doi.org/10.1016/j.bbrc.2015.03.129

Hsiao, K. Y., Sun, H. S., Tsai, S. J. (2017). Circular RNA - new member of noncoding RNA with novel function. Exp. Biol. Med., 242 (11), 1136-1141. DOI: https://doi.org/10.1177/1535370217708978

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

Ikeda, S., Kong, S. W., Bisping, E. et al. (2007). Altered microRNA expression in human heart diseases. Physiol Genomics, 31 (3), 367-373. DOI: https://doi.org/10.1152/physiolgenomics.00144.2007

Karakikes, I., Chaanine, A. H., Kang, S. et al. (2013). Therapeutic cardiac-targeted delivery of miR-1 reverses pressure overload-induced cardiac hypertrophy. J. Amer. Heart Assoc., 2 (2), e 00078.

Kim, J. O., Song, D. W., Kwon, E. J. et al. (2015). MiR-185 play an anti-hypertrophic role in the heart via multiple targets in the calcium-signaling pathways. PLoS One, 10 (3), e 122309. DOI: https://doi.org/10.1371/journal.pone.0122509

Latronico, M. V., Condorelli, G. (2015). Therapeutic application of nonconding RNAS. Curr. Opin. Cardiol., 30 (3), 213-221. DOI: https://doi.org/10.1097/HCO.0000000000000162

Lekka, E., Hall, J. (2018). Noncoding RNAS in disease. FEBS Lett., 592 (17), 2884-2900. DOI: https://doi.org/10.1002/1873-3468.13182

Li, Q., Song, X. W., Zon, J. et al. (2010). Attenuation of microRNA-1 derepresses the cytoskeleton regulatory protein twinfilin-1 to provoke cardiac hypertrophy. J. Cell. Sci., 123 (p+14), 2444-2452. DOI: https://doi.org/10.1242/jcs.067165

Li, R., Yan, G., Zhang, Q. et al. (2013). MiR-145 inhibits isoproterenol-induced cardiomyocite hypertrophy by targeting the expression and localization of GATA6. FEBS Lett., 587 (12), 1754-1761. DOI: https://doi.org/10.1016/j.febslet.2013.04.018

Li, Z., Song, Y., Liu, L. et al. (2017). MiR-199a impairs autophagy and induces cardiac hypertrophy through mTOR activatios. Cell Death Differ., 24 (7), 1205-1213. DOI: https://doi.org/10.1038/cdd.2015.95

Li, X., Zeng, Z., Li, Q. et al. (2015). Inhibition of microRNA-497 ameliorates anoxia/reoxygenation injury in cardiomyocytes by suppressing cell apoptosis and enhancing autophagy. Oncotarget, 6 (22), 1882818844. DOI: https://doi.org/10.18632/oncotarget.4774

Liu, L., Zhang, G., Liang, Z. et al. (2014). MicroRNA-156 enhances hypoxia/reoxygenation induced apoptosis of cardiomyocytes via amitochondrial apoptoticpathway. Apoptosis, 19 (1), 19-29 DOI: https://doi.org/10.1007/s10495-013-0899-2

Matkovich, S. J., Van Booven, D. J., Yonker, K. A. et al. (2009). Reciprocal regulation of myocardial microRNAS and messenger RNA in human cardiomyopathy and reversal of the microRNA signature by biomechanical support. Circulation, 119 (9), 1263-1271. DOI: https://doi.org/10.1161/CIRCULATIONAHA.108.813576

Matkovich, S. J., Wang, W., Tu, Y. et al. (2010). MicroRNA-133a protects against myocardial fibrosis and modulates electrical repolarization without affecting hypertrophy in pressure-overload adult hearts. Circ. Res., 106 (1), 166-175. DOI: https://doi.org/10.1161/CIRCRESAHA.109.202176

Maraoka, N., Yamakawa, H., Miyamoto, K. et al. (2014). MiR-133 promotes cardiac reprogramming by directly repressing Snai 1 and sieencing fibroblast signatures. EMBO J., 33 (14), 1565-1581. DOI: https://doi.org/10.15252/embj.201387605

Naga Prasad, S. V., Dnan, Z. H., Gupta, M. K. et al. (2009). Unique microRNA profile in end-stage heart failure indicates alterations in specific cardiovascular signaling network. J. Biol. Chem., 284 (40), 2748727499. DOI: https://doi.org/10.1074/jbc.M109.036541

Nagpal, V., Rai, R., Place, A. T. et al. (2016). MiR-125b is critical of fibroblast-to-myofibroblast transition and cardiac fibrosis. Circulation, 133 (3), 291-301. DOI: https://doi.org/10.1161/CIRCULATIONAHA.115.018174

Pan, Z., Sun, X., Ren, J. et al. (2012). MicroRNA-101 inhibited postinfaret cardiac fibrosis. Circulation, 126 (7), 840-850. DOI: https://doi.org/10.1161/CIRCULATIONAHA.112.094524

Pan, Z., Sun, X., Ren J. et al. (2012). MiR-1 exacerkates cardiac ischemia - reperfusion injury in mouse models. PLoS One, 7 (11), e50515. DOI: https://doi.org/10.1371/journal.pone.0050515

Pan, L., Huang, B. J., Ma, X. E. et al. (2015). MiR-25 protects cardiomyocytes against oxidative damage by targeting the mitochondrial calcium uniporter. Int. J. Mol. Sci., 16 (3), 5420-5433. DOI: https://doi.org/10.3390/ijms16035420

Rane, S., He, M., Sayed, D. et al. (2009). Downregulation of miR-199a derepresses hypoxia-inducible factor-alpha and sirtuinl and recapitulates hypoxia preconditioning in cardiac myocytes. Circ. Res., 104 (7), 879-886. DOI: https://doi.org/10.1161/CIRCRESAHA.108.193102

Roca-Alonso, L., Caslellano, L., Mils, A. et al. (2015). Myocardyol miR-30 down regulation triggered by doxorubiun drives alteration in в-adrenerfic signaling and enhances apoptosis. Cell Death Dis., 6, e1754. DOI: https://doi.org/10.1038/cddis.2015.89

Rov, S., Khanna, S., Hussain, S. R. et al. (2009). MicroRNA expression in responcse to murine myocardial infarction: miR-21 regulates fibroblast metalloprotease-2 via phosphatase and teasin homologue. Cardiovase. Res., 82 (1), 21-29.

Sathyamangla, V., Naga Prasad, S. V., Karnik, S. S. (2010). MicroRNAS - regulators of signaling networks in dilated cardiomyopathy. J. Cardiovasc. Transl. Res., 3 (3), 225-234.

Sayed, D., Hong, C., Chen, I. Y. et al. (2007). MicroRNAS play an essential role in development of cardiac hyperthrophy. Circ. Res., 100 (3), 416-424. DOI: https://doi.org/10.1161/01.RES.0000257913.42552.23

Shrestha, A., Mukhametshina, R. T., Taghiradeh, S. et al. (2017). MicroRNA-142 is a multifaceted regulator in ergemogenesis, homeostasis and dispase. Dev. Dyn., 246 (4), 285-290. DOI: https://doi.org/10.1002/dvdy.24477

Song, D. W., Ryu, J. K., Kim, J. O. et al. (2014). The miR-19a/b family positively regulates cardiomyocyte hypertrophy by targeting atrogin-1. Biochem. J., 457 (1), 151-162. DOI: https://doi.org/10.1042/BJ20130833

Song, S., Seo, H. H., Lee, S. Y. et al. (2015). MicroRNA-17 - mediated down-regulation of apoptotic APAF1 atennates apoptosome formation in cardiomyocytes. Biochem. Biophys. Res. Commun., 465 (2), 299-304. DOI: https://doi.org/10.1016/j.bbrc.2015.08.028

Thum, T., Gross, C., Fiedler, J. et al. (2008). MicroRNA-21 contributes to myocardial disease by stimulation MAP kinase signaling in fibroblasts. Nature, 456 (7224), 980-984.

Tu, Y., Wan, L., Bu, L. et al. (2013). MicroRNA-22 downregulation by atorvastation in a mouse model of csrdiac hypertrophy. Cell Physiol. Biochem., 31 (6), 997-1008. DOI: https://doi.org/10.1159/000350117

Usar, A., Gupta, S. K., Fiedeer, J. et al. (2012). The miRNA-212/132 family regulates both cardiac hypertrophy and autophagy in cardiomyocytes. Nat. Commun., 3, 1078.

Vakron, S., Fukunage, R., Foster, B. et al. (2018). Allele-specific differences in transcriptome, miRNome, and mitochondrial function in two hypertrophic cardiomyopathy. JCI Insight., 3 (6), e94493.

Van Rooij, E., Sutherland, L. B., Thatcher, J. E. et al. (2008). Dysregulation of microRNAS after myocardial infarction releals a role miR-29 in cardiac fibrosis. Proc. Natl. Acad. Sci., 105 (35), 13027-13032. DOI: https://doi.org/10.1073/pnas.0805038105

Volk, N., Paul, E. D., Haramati, S. et al. (2014). MicroRNA-19b associates with Ago2 in a migdala following chronic stress. J. Neurosci., 34 (45), 1507015082.

Wang, C., Wang, S., Zhao, P. et at. (2012). MiR-221 promotes cardiac hypertrophy in vitro through the modulation of p27 expression. J. Cell Biochem., 113 (6), 2040-2046. DOI: https://doi.org/10.1002/jcb.24075

Wang, J., Song, Y., Zhang, Y. et al. (2012). Cardiomyocyte overexpression of miR-276 inducer cardiac hypertrophy and dysfuntion in mice. Cell Res., 22 (3), 516-527. DOI: https://doi.org/10.1038/cr.2011.132

Wang, J., Huang, W., Xu, R. et al. (2012). MicroRNA-24 regulates cardiac fibrosis after myocardial infarction. J. Cell Mol. Med., 16 (9), 2150-2160. DOI: https://doi.org/10.1111/j.1582-4934.2012.01523.x

Wang, J., Liew, O. W., Richards, A. M. et al. (2016). Owerview of microRNAS in cardiac hypertrophy, fibrosis and apoptosis. Int. J. Mol. Sci., 17 (5), 749.

Wang, K., Long, B., Zhon, J., Li, P. F. (2010). MiR-9 and NFATc3 regulate myocardin in cardiac hypertrophy. J. Biol. Chem., 285 (16), 11903-11912. DOI: https://doi.org/10.1074/jbc.M109.098004

Wang, K., Lin, Z. Q., Long, B. et al. (2012). Cardiac hypertrophy is positively regulated by microRNA mir-23a. J. Biol. Chem., 287 (1), 589-599. DOI: https://doi.org/10.1074/jbc.M111.266940

Wang, X., Wang, H. X., Li, Y. L. et al. (2015). MicroRNA Let-7i negatively regulates cardiac inflammation and fibrosis. Hypertension, 66 (4), 776-785. DOI: https://doi.org/10.1161/HYPERTENSIONAHA.115.05548

Wei, C., Kim, I. K., Kumar, S. et al. (2013). NF-kB mediated miR-26a regulation in cardiac fibrosis. J. Cell Physiol., 228 (7), 1433-1443. DOI: https://doi.org/10.1002/jcp.24296

Wei, C., Li, L., Gupta, S. (2014). NF-kB - mediated miR-30b regulation in cardiomyocytes cell death by targeting Bel-2. Mol. Cell Biochem., 387 (1-2), 135-141. DOI: https://doi.org/10.1007/s11010-013-1878-1

Wei, L., Yaan, M., Zhon, R. et al. (2015). MicroRNA-101 in hibits rat cardiac hypertrophy by targenting Rab 1a. J. Cardiovasc. Pharmacol., 65 (4), 357-363. DOI: https://doi.org/10.1097/FJC.0000000000000203

Xu, C., Hu, Y., Hou, L. et al. (2014). fi-bloker carvedilol protects cardiomyocytes against exidative stress -induced apoptosis by up-regulating miR-133 expression. J. Mol. Cell Cardiol., 75, 111-121. DOI: https://doi.org/10.1016/j.yjmcc.2014.07.009

Xue, M., Zhuo, Y., Shau, B. (2017). microRNAS; long noncoding RNAS and their function in human disease. Methods Mol. Biol., 1617, 1-25.

Yang, Y., Ago, T., Zhai, P. et al. (2011). Thioredoxin 1 negatively regulates angiotensin II-induced cardiac hypertrophy through upregulation of miR-98/Let7. Circ. Res., 108 (3), 305-315. DOI: https://doi.org/10.1161/CIRCRESAHA.110.228437

Yang, J., Nie, Y., Wang, F. et al. (2013). Reciprocal regulation of miR-23a and lypophosphatidic acid-receptor signaling in cardiomyocyte hypertrophy. Biochem. Biophys. Acta., 183 (8), 1386-1394.

Yang, Q., Yang, K., Li, A. (2014). MicroRNA-21 protects against ischemia-reperfusion and hypoxia-reperfusion-induced apoptosis via the phosphatap and tensin homolog/Akt-dependent mechanism. Mol. Med. Rep., 9 (6), 2213-2220. DOI: https://doi.org/10.3892/mmr.2014.2068

Zhao, F., Li, B., Wei, Y. Z. et al. (2013). MicroRNA-34a regulates high gluase-induced apoptosis in H9c2 cardiomyocytes. J. Huazhong Univ. Sci. Technolog. Med. Sci., 33 (6), 834-839. DOI: https://doi.org/10.1007/s11596-013-1207-7

Zhao, X., Wang, K., Liao, Y. et al. (2015). MicroRNA-101a inhibits cardiac fibrosis induced by hypoxia via targeting TGFfiR1 on cardiac fibroblasts. Cell Physiol. Biochem., 35 (1), 213-226. DOI: https://doi.org/10.1159/000369689

Zhao, Y., Ransom, J. F., Li, A. et al. (2007). Dysregulation of cardiogenesis: cardiac conduction, and cell cycle in mice lacking miRNA-1-2. Cell, 129 (2), 303-317. DOI: https://doi.org/10.1016/j.cell.2007.03.030

Zhang, Y., Huang, X. R., Wei, L. H. et al. (2014). MiR-29b as a therapeutic agents for angiotensin II- induced cardiac fibrosis by targeting TGF-p/Smad3 signaling. Mol. Ther., 22 (5), 974-985. DOI: https://doi.org/10.1038/mt.2014.25

Allmer, J., Yousef, M. (2016). Computational miRNomics. Journal of Integrative Bioinformatics, 13 (5), 1-2. DOI: https://doi.org/10.1515/jib-2016-302

Published

2019-09-30

How to Cite

Mintser, O. P., & Zaliskyi, V. M. (2019). SYSTEMS INTERACTION microRNAs IN PATHOGENESIS OF CARDIOVASCULAR DISEASES. Medical Informatics and Engineering, (3), 4–19. https://doi.org/10.11603/mie.1996-1960.2019.3.10428

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