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AntimiR-132 Attenuates Myocardial Hypertrophy in an Animal Model of Percutaneous Aortic Constriction.
- Source :
-
Journal of the American College of Cardiology (JACC) . Jun2021, Vol. 77 Issue 23, p2923-2935. 13p. - Publication Year :
- 2021
-
Abstract
- <bold>Background: </bold>Pathological cardiac hypertrophy is a result of afterload-increasing pathologies including untreated hypertension and aortic stenosis. It features progressive adverse cardiac remodeling, myocardial dysfunction, capillary rarefaction, and interstitial fibrosis often leading to heart failure.<bold>Objectives: </bold>This study aimed to establish a novel porcine model of pressure-overload-induced heart failure and to determine the effect of inhibition of microribonucleic acid 132 (miR-132) on heart failure development in this model.<bold>Methods: </bold>This study developed a novel porcine model of percutaneous aortic constriction by implantation of a percutaneous reduction stent in the thoracic aorta, inducing progressive remodeling at day 56 (d56) after pressure-overload induction. In this study, an antisense oligonucleotide specifically inhibiting miR-132 (antimiR-132), was regionally applied via intracoronary injection at d0 (percutaneous transverse aortic constriction induction) and d28.<bold>Results: </bold>At d56, antimiR-132 treatment diminished cardiomyocyte cross-sectional area (188.9 ± 2.8 vs. 258.4 ± 9.0 μm2 in untreated hypertrophic hearts) and improved global cardiac function (ejection fraction 48.9 ± 1.0% vs. 36.1 ± 1.7% in control hearts). Moreover, at d56 antimiR-132-treated hearts displayed less increase of interstitial fibrosis compared with sham-operated hearts (Δsham 1.8 ± 0.5%) than control hearts (Δsham 10.8 ± 0.6%). Of note, cardiac platelet and endothelial cell adhesion molecule 1+ capillary density was higher in the antimiR-132-treated hearts (647 ± 20 cells/mm2) compared with in the control group (485 ± 23 cells/mm2).<bold>Conclusions: </bold>The inhibition of miR-132 is a valid strategy in prevention of heart failure progression in hypertrophic heart disease and may be developed as a treatment for heart failure of nonischemic origin. [ABSTRACT FROM AUTHOR]
- Subjects :
- *CARDIAC hypertrophy
*HEART failure
*CELL adhesion molecules
*HEART diseases
*THORACIC aorta
*SKIN absorption
*ANIMAL models in research
*MUSCULAR hypertrophy
*RNA metabolism
*BIOLOGICAL models
*RESEARCH
*AORTIC diseases
*VENTRICULAR remodeling
*STENOSIS
*ANIMAL experimentation
*RESEARCH methodology
*RNA
*SWINE
*SURGICAL stents
*MEDICAL cooperation
*EVALUATION research
*TREATMENT effectiveness
*COMPARATIVE studies
*CORONARY arteries
*INTRA-arterial injections
*DISEASE complications
Subjects
Details
- Language :
- English
- ISSN :
- 07351097
- Volume :
- 77
- Issue :
- 23
- Database :
- Academic Search Index
- Journal :
- Journal of the American College of Cardiology (JACC)
- Publication Type :
- Academic Journal
- Accession number :
- 150874371
- Full Text :
- https://doi.org/10.1016/j.jacc.2021.04.028