| http://purl.uniprot.org/citations/23612897 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/23612897 | http://www.w3.org/2000/01/rdf-schema#comment | "BackgroundMicroRNAs (miRNAs) play a key role in the development of heart failure, and recent studies have shown that the muscle-specific miR-1 is a key regulator of cardiac hypertrophy. We tested the hypothesis that chronic restoration of miR-1 gene expression in vivo will regress hypertrophy and protect against adverse cardiac remodeling induced by pressure overload.Methods and resultsCardiac hypertrophy was induced by left ventricular pressure overload in male Sprague-Dawley rats subjected to ascending aortic stenosis. When the hypertrophy was established at 2 weeks after surgery, the animals were randomized to receive either an adeno-associated virus expressing miR-1 (AAV9.miR-1) or green fluorescent protein (GFP) as control (AAV9.GFP) via a single-bolus tail-vein injection. Administration of miR-1 regressed cardiac hypertrophy (left ventricular posterior wall thickness,; 2.32±0.08 versus 2.75±0.07 mm, P<0.001) and (left ventricular septum wall thickness, 2.23±0.06 versus 2.54±0.10 mm, P<0.05) and halted the disease progression compared with control-treated animals, as assessed by echocardiography (fractional shortening, 37.60±5.01% versus 70.68±2.93%, P<0.05) and hemodynamic analyses (end-systolic pressure volume relationship/effective arterial elastance, 1.87±0.46 versus 0.96±0.38, P<0.05) after 7 weeks of treatment. Additionally, miR-1 replacement therapy lead to a marked reduction of myocardial fibrosis, an improvement in calcium handling, inhibition of apoptosis, and inactivation of the mitogen-activated protein kinase signaling pathways, suggesting a favorable effect on preventing the maladaptive ventricular remodeling. We also identified and validated a novel bona fide target of miR-1, Fibullin-2 (Fbln2), a secreted protein implicated in extracellular matrix remodeling.ConclusionsTaken together, our findings suggest that restoration of miR-1 gene expression is a potential novel therapeutic strategy to reverse pressure-induced cardiac hypertrophy and prevent maladaptive cardiac remodeling."xsd:string |
| http://purl.uniprot.org/citations/23612897 | http://purl.org/dc/terms/identifier | "doi:10.1161/jaha.113.000078"xsd:string |
| http://purl.uniprot.org/citations/23612897 | http://purl.uniprot.org/core/author | "Kang S."xsd:string |
| http://purl.uniprot.org/citations/23612897 | http://purl.uniprot.org/core/author | "Zhang S."xsd:string |
| http://purl.uniprot.org/citations/23612897 | http://purl.uniprot.org/core/author | "Jeong D."xsd:string |
| http://purl.uniprot.org/citations/23612897 | http://purl.uniprot.org/core/author | "Hajjar R.J."xsd:string |
| http://purl.uniprot.org/citations/23612897 | http://purl.uniprot.org/core/author | "Karakikes I."xsd:string |
| http://purl.uniprot.org/citations/23612897 | http://purl.uniprot.org/core/author | "Lebeche D."xsd:string |
| http://purl.uniprot.org/citations/23612897 | http://purl.uniprot.org/core/author | "Chaanine A.H."xsd:string |
| http://purl.uniprot.org/citations/23612897 | http://purl.uniprot.org/core/author | "Mukete B.N."xsd:string |
| http://purl.uniprot.org/citations/23612897 | http://purl.uniprot.org/core/date | "2013"xsd:gYear |
| http://purl.uniprot.org/citations/23612897 | http://purl.uniprot.org/core/name | "J Am Heart Assoc"xsd:string |
| http://purl.uniprot.org/citations/23612897 | http://purl.uniprot.org/core/pages | "e000078"xsd:string |
| http://purl.uniprot.org/citations/23612897 | http://purl.uniprot.org/core/title | "Therapeutic cardiac-targeted delivery of miR-1 reverses pressure overload-induced cardiac hypertrophy and attenuates pathological remodeling."xsd:string |
| http://purl.uniprot.org/citations/23612897 | http://purl.uniprot.org/core/volume | "2"xsd:string |
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| http://purl.uniprot.org/uniprot/#_B7Z6T9-mappedCitation-23612897 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/23612897 |
| http://purl.uniprot.org/uniprot/#_B7Z9B8-mappedCitation-23612897 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/23612897 |
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| http://purl.uniprot.org/uniprot/#_P98095-mappedCitation-23612897 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/23612897 |