ArticleMolecular therapy. Methods & clinical development2024
Protein phosphatase 2A anchoring disruptor gene therapy for familial dilated cardiomyopathy.
Article in Molecular therapy. Methods & clinical development, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed, 1 citations in OpenAlex.
- AKAP6β-a conductor in the orchestra of pathological cardiomyocyte gene transcription.Molecular pharmacology · 2026Review
- FAMILIAL CARDIOMYOPATHY IN NIGERIA: A CASE REPORT.Annals of Ibadan postgraduate medicine · 2026Article
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Authors and funding
5 authors at 1 institution in 1 country.
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Abstract
Familial dilated cardiomyopathy is a prevalent cause of heart failure that results from the mutation of genes encoding proteins of diverse function. Despite modern therapy, dilated cardiomyopathy typically has a poor outcome and is the leading cause of cardiac transplantation. The phosphatase PP2A at cardiomyocyte perinuclear mAKAPβ signalosomes promotes pathological eccentric cardiac remodeling, as is characteristic of dilated cardiomyopathy. Displacement of PP2A from mAKAPβ, inhibiting PP2A function in that intracellular compartment, can be achieved by expression of a mAKAPβ-derived PP2A binding domain-derived peptide. To test whether PP2A anchoring disruption would be effective at preventing dilated cardiomyopathy-associated cardiac dysfunction, the adeno-associated virus gene therapy vector AAV9sc.PBD was devised to express the disrupting peptide in cardiomyocytes
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