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| Bioinformatics analysis of the relationship between miRNA-494 and myocardial fibrosis in chronic heart failure |
| LIANG Shan1 HE Yazhou1 LI Lijuan1 HUANG Caiyi1 WANG Qinggao2 |
1.Graduate School, Guangxi University of Chinese Medicine, Guangxi Zhuang Autonomous Region, Nanning 530001, China;
2.Department of Cardiology, the First Affiliated Hospital of Guangxi University of Chinese Medicine, Guangxi Zhuang Autonomous Region, Nanning 530023, China |
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Abstract Objective To explore the mechanism of myocardial fibrosis in chronic heart failure patients by using bioinformatics analysis. Methods The GSE104150 dataset through GEO database was filtered out, the differentially expressed miRNAs between heart failure and healthy control was analyzed. The target genes of miR-494 were predicted, which should be performed the gene ontology (GO) enrichment analysis and signal pathway enrichment analysis. Results Compared with the healthy control, miRNA-494 was differentially expressed in the chronic heart failure patients. The GO analysis showed the target genes of miR-494 were enriched in cell components such as cytoplasm and nucleus, molecular functions as protein binding and biological functions as cell proliferation and migration, phosphatidylinositol-mediated signaling. The KEGG biological pathway was mainly enriched in TGFβ, PI3K/Akt, and MAPK signaling pathways. Conclusion It is speculated that miRNA-494 is differentially expressed in patients with chronic heart failure, and it has a certain correlation with the occurrence and development of myocardial fibrosis, further research is needed to confirm.
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[1] Huntzinger E，Izaurralde E. Gene silencing by microRNAs：contributions of translational repression and mRNA decay [J]. Nat Rev Genet，2011，12（2）：99-110.
[2] Xu J，Shao T，Ding N，et al. miRNA-miRNA crosstalk：from genomics to phenomics [J]. Brief Bioinform，2017，18（6）：1002-1011.
[3] Verjans R，Peters T，Beaumont FJ，et al. MicroRNA-221/222 Family Counteracts Myocardial Fibrosis in Pressure Overload-Induced Heart Failure [J]. Hypertension，2018， 71（2）：280-288.
[4] Shyu KG，Wang BW，Cheng WP，et al. MicroRNA-208a Increases Myocardial Endoglin Expression and Myocardial Fibrosis in Acute Myocardial Infarction [J]. Can J Cardiol Can J Cardiol，2015，31（5）：679-690.
[5] Qian W，Xin S，Rui C，et al. Ghrelin Ameliorates Angiotensin Ⅱ-Induced Myocardial Fibrosis by Upregulating Peroxisome Proliferator-Activated Receptor Gamma in Young Male Rats [J]. Biomed Res Int，2018，2018：1-14.
[6] Roy C，Slimani A，de Meester C，et al. Associations and prognostic significance of diffuse myocardial fibrosis by cardiovascular magnetic resonance in heart failure with preserved ejection fraction [J]. J Cardiovasc Magn Reson，2018，20（1）：55.
[7] Weber KT，Díez J. Targeting the Cardiac Myofibroblast Secretome to Treat Myocardial Fibrosis in Heart Failure [J]. Circ Heart Fail，2016，9（8）：e003315.
[8] Heinzmann D，Fu?覻 S，Ungern-Sternberg SV，et al. TGFβ Is Specifically Upregulated on Circulating CD14++ CD16+ and CD14+ CD16++ Monocytes in Patients with Atrial Fibrillation and Severe Atrial Fibrosis [J]. Cell Physiol Biochem，2018，49（1）：226-234.
[9] Iyer RP，Patterson NL，Fields GB，et al. The history of matrix metalloproteinases：milestones，myths，and misperceptions [J]. Am J Physiol Heart Circ Physiol，2012，303（8）：H919-H930.
[10] Sun T，Cheung KSC，Liu ZL，et al. Matrix metallopeptidase 9 targeted by hsa-miR-494 promotes silybin-inhibited osteosarcoma [J]. Mol Carcinog，2018，57（2）：262-271.
[11] M?觟hnle P，Schütz SV，Schmidt M，et al. MicroRNA-665 is involved in the regulation of the expression of the cardioprotective cannabinoid receptor CB2 in patients with severe heart failure [J]. Biochem Biophys Res Commun，2014，451（4）：516-521.
[12] Heger J，Schulz R，Euler G，et al. Molecular switches under TGFβ signalling during progression from cardiac hypertrophy to heart failure [J]. Br J Pharmacol，2016，173（1）：3-14.
[13] Li L，Zhao D，Jin Z，et al. Phosphodiesterase 5a Inhibition with Adenoviral Short Hairpin RNA Benefits Infarcted Heart Partially through Activation of Akt Signaling Pathway and Reduction of Inflammatory Cytokines [J]. PLoS One，2015，10（12）：e0145766.
[14] Li SC，Ma LN，Chen J，et al. Effect of allicin on myocardial fibrosis after myocardial infarction in rats and its relationship with TGFβ/Smads signal transduction [J]. Zhongguo Zhong Yao Za Zhi，2016，41（13）：2517-2521.
[15] Huang C，Du R，Zhang P，et al. Expression，purification，and functional characterization of recombinant PTD-SARA [J]. Acta Biochim Biophys Sin （Shanghai），2011， 43（2）：110-117.
[16] Williams SM，Golden-Mason L，Ferguson BS，et al. Class I HDACs regulate angiotensin Ⅱ-dependent cardiac fibrosis via fibroblasts and circulating fibrocytes [J]. J Mol Cell Cardiol，2014，67：112-125.
[17] Liu M，Li Z，Liang B，et al. Hydrogen sulfide ameliorates rat myocardial fibrosis induced by thyroxine through PI3K/AKT signaling pathway [J]. Endocr J，2018，65（7）：769-781.
[18] Morine KJ，Qiao X，York S，et al. Bone Morphogenetic Protein 9 Reduces Cardiac Fibrosis and Improves Cardiac Function in Heart Failure [J]. Circulation，2018，138（5）：513-526.
[19] Li L，Fang C，Xu D，et al. Cardiomyocyte specific deletion of PP2A causes cardiac hypertrophy [J]. Am J Transl Res，2016，8（4）：1769-1779.
[20] Zhang Y，Gao F，Tang Y，et al. Valproic acid regulates Ang Ⅱ-induced pericyte-myofibroblast trans-differentiation via MAPK/ERK pathway [J]. Am J Transl Res，2018，10（7）：1976-1989.
[21] Lee J，Levin DE. Intracellular mechanism by which arsenite activates the yeast stress MAPK Hog1 [J]. Mol Biol Cell，2018，29（15）：1904-1915.
[22] Tian J，Zhao Y，Liu Y，et al. Roles and Mechanisms of Herbal Medicine for Diabetic Cardiomyopathy：Current Status and Perspective [J]. Oxid Med Cell Longev，2017， 2017：8214541.
[23] Reyes DRA，Gomes MJ，Rosa CM，et al. N-Acetylcysteine Influence on Oxidative Stress and Cardiac Remodeling in Rats During Transition from Compensated Left Ventricular Hypertrophy to Heart Failure [J]. Cell Physiol Biochem，2017，44（6）：2310-2321. |
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