| http://purl.uniprot.org/citations/33982231 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/33982231 | http://www.w3.org/2000/01/rdf-schema#comment | "Increased histone deacetylase 3 (HDAC3) has been demonstrated to contribute to the pathogenesis of myocardial ischemia-reperfusion injury (MI/RI). Therefore, the goal of this study was to investigate how HDAC3 regulated MI/RI by mediating microRNA (miR)-494-3p/dromodomain-containing protein 4 (BRD4) axis. The MI/RI model was established by ligating the right anterior descending coronary artery. Cardiomyocytes from newborn mice were treated with hypoxia/reoxygenation (H/R). Gain-of-function and loss-of-function approaches were implemented to figure out the roles of miR-494-3p and HDAC3 in MI/RI. miR-494-3p, HDAC3, and BRD4 in myocardial tissues of mice with MI/RI and H/R-treated cardiomyocytes were detected. The relationships between miR-494-3p and HDAC3 and BRD4 were identified. Reduced miR-494-3p and upregulated HDAC3 and BRD4 exhibited in myocardial tissues of mice with MI/RI and H/R-treated cardiomyocytes. Inhibited HDAC3 or elevated miR-494-3p repressed the inflammation and apoptosis, improved cardiac function, and ameliorated myocardial injury in myocardial tissues of mice with MI/RI. Suppression of HDAC3 or elevation of miR-494-3p depressed inflammation and apoptosis and promoted cell viability of primary cardiomyocytes. miR-494-3p targeted BRD4. The study concludes that suppressed HDAC3 plays a protective role in MI/RI by upregulation of miR-494-3p and inhibition of BRD4, which could be helpful for MI/RI therapy."xsd:string |
| http://purl.uniprot.org/citations/33982231 | http://purl.org/dc/terms/identifier | "doi:10.1007/s12035-021-02369-y"xsd:string |
| http://purl.uniprot.org/citations/33982231 | http://purl.uniprot.org/core/author | "Fang L."xsd:string |
| http://purl.uniprot.org/citations/33982231 | http://purl.uniprot.org/core/author | "Li J."xsd:string |
| http://purl.uniprot.org/citations/33982231 | http://purl.uniprot.org/core/author | "Li W."xsd:string |
| http://purl.uniprot.org/citations/33982231 | http://purl.uniprot.org/core/author | "Zhang Z."xsd:string |
| http://purl.uniprot.org/citations/33982231 | http://purl.uniprot.org/core/author | "Zheng W."xsd:string |
| http://purl.uniprot.org/citations/33982231 | http://purl.uniprot.org/core/author | "Xie Q."xsd:string |
| http://purl.uniprot.org/citations/33982231 | http://purl.uniprot.org/core/date | "2021"xsd:gYear |
| http://purl.uniprot.org/citations/33982231 | http://purl.uniprot.org/core/name | "Mol Neurobiol"xsd:string |
| http://purl.uniprot.org/citations/33982231 | http://purl.uniprot.org/core/pages | "4268-4279"xsd:string |
| http://purl.uniprot.org/citations/33982231 | http://purl.uniprot.org/core/title | "Inhibited HDAC3 or Elevated MicroRNA-494-3p Plays a Protective Role in Myocardial Ischemia-Reperfusion Injury via Suppression of BRD4."xsd:string |
| http://purl.uniprot.org/citations/33982231 | http://purl.uniprot.org/core/volume | "58"xsd:string |
| http://purl.uniprot.org/citations/33982231 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/33982231 |
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