ArticleMolecular therapy : the journal of the American Society of Gene Therapy2014
Cardiac I-1c overexpression with reengineered AAV improves cardiac function in swine ischemic heart failure.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 83 citations in OpenAlex.
- Are RNA Therapies a Solid Foundation or a Frontier Yet to Be Conquered?International journal of molecular sciences · 2026Review
- Macrophage-specific circular RNA circHIPK2, inflammation, and fibrosis after myocardial infarction.European heart journal · 2026Article
- Past, Present and Future of Regenerative Gene Therapy for Ischemic Heart Failure.Journal of cardiovascular translational research · 2026Review
- High-throughput evaluation of cardiac-specific promoters for adeno-associated virus mediated cardiac gene therapy.Gene therapy · 2026Article
- Gene Therapy for Heart Failure.Journal of cardiovascular translational research · 2026Review
- Gene Therapy for Heart Failure: Impact on Mitochondrial Dysfunction.Biomedicines · 2026Review
- Cardiotropic AAV gene therapy for heart failure: a phase 1 trial.Nature medicine · 2025Article
- Gene therapy in cardiac and vascular diseases: a review of approaches to treat genetic and common cardiovascular diseases with novel gene-based therapeutics.Cardiovascular research · 2025Review
- PERM1 Gene Delivery via AAV Prevents Heart Failure in a Mouse Model of Pressure Overload.bioRxiv : the preprint server for biology · 2025Article
- State of the art and perspectives of gene therapy in heart failure. A scientific statement of the Heart Failure Association of the ESC, the ESC Council on Cardiovascular Genomics and the ESC Working Group on Myocardial & Pericardial Diseases.European journal of heart failure · 2025Review
- Non-Coding RNA-Targeted Therapy: A State-of-the-Art Review.International journal of molecular sciences · 2024Review
- Hypertrophic Cardiomyopathy versus Storage Diseases with Myocardial Involvement.International journal of molecular sciences · 2023Review
- Extracellular Vesicle-Encapsulated Adeno-Associated Viruses for Therapeutic Gene Delivery to the Heart.Circulation · 2023Article
- Barriers in Heart Failure Gene Therapy and Approaches to Overcome Them.Heart, lung & circulation · 2023Article
- Progress in Clinical Gene Therapy for Cardiac Disorders.Molecular diagnosis & therapy · 2023Review
- Therapeutic efficacy of AAV-mediated restoration of PKP2 in arrhythmogenic cardiomyopathy.Nature cardiovascular research · 2023Article
- Gene Therapy and Cardiovascular Diseases.Advances in experimental medicine and biology · 2023Article
- Distribution of cardiomyocyte-selective adeno-associated virus serotype 9 vectors in swine following intracoronary and intravenous infusion.Physiological genomics · 2022Article
- MicroRNAs as therapeutic targets in cardiovascular disease.The Journal of clinical investigation · 2022Review
- A review of the underlying genetics and emerging therapies for canine cardiomyopathies.Journal of veterinary cardiology : the official journal of the European Society of Veterinary Cardiology · 2022Review
Corrections and comments
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Authors and funding
20 authors at 6 institutions in 1 country.
Funding
Abstract
Cardiac gene therapy has emerged as a promising option to treat advanced heart failure (HF). Advances in molecular biology and gene targeting approaches are offering further novel options for genetic manipulation of the cardiovascular system. The aim of this study was to improve cardiac function in chronic HF by overexpressing constitutively active inhibitor-1 (I-1c) using a novel cardiotropic vector generated by capsid reengineering of adeno-associated virus (BNP116). One month after a large anterior myocardial infarction, 20 Yorkshire pigs randomly received intracoronary injection of either high-dose BNP116.I-1c (1.0 × 10(13) vector genomes (vg), n = 7), low-dose BNP116.I-1c (3.0 × 10(12) vg, n = 7), or saline (n = 6). Compared to baseline, mean left ventricular ejection fraction increased by 5.7% in the high-dose group, and by 5.2% in the low-dose group, whereas it decreased by 7% in the saline group. Additionally, preload-recruitable stroke work obtained from pressure-volume analysis demonstrated significantly higher cardiac performance in the high-dose group. Likewise, other hemodynamic parameters, including stroke volume and contractility index indicated improved cardiac function after the I-1c gene transfer. Furthermore, BNP116 showed a favorable gene expression pattern for targeting the heart. In summary, I-1c overexpression using BNP116 improves cardiac function in a clinically relevant model of ischemic HF.
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