ArticleFundamental research2025
Myocardial infarction creates a critical time window for AAV-based cardiac gene transfer.
Article in Fundamental research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Cardiac-targeting peptide-modified Prussian blue nanozymes loaded with Astragaloside IV for efficient ICI-myocarditis therapy.Materials today. Bio · 2026Article
- Cardiomyocyte-Derived USP20 Attenuates Diabetic Cardiomyopathy by Facilitating the Degradation of STING and Mitigating STING-Mediated Inflammation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Exploring Phosphatase and Tensin Homologue Deleted on Chromosome Ten (PTEN) as a Potential Therapeutic Target for Cardiac Hypertrophy.ACS pharmacology & translational science · 2025Review
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Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Approaches to enhance adeno-associated virus (AAV)-based cardiac gene transfer are the key to successful cardiac gene therapy, but factors influencing AAV transduction remain poorly investigated. This study showed that myocardial infarction (MI) enhanced cardiac AAV transduction, peaking at the third day post-MI in mice. The excessive AAV enrichment at the border zone is due to local vascular permeabilization and cardiomyocyte metabolic remodeling, which is independent of AAV dosage, serotypes and promoters. This effect was harnessed to boost cardiac base editing and improve the outcome of gene therapy for MI in mice. Thus, heart disease itself is a non-negligible factor that alters AAV-based cardiac gene transfer, which provides a new inroad to develop approaches to enhance cardiac gene therapy.
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