ArticleThe Journal of thoracic and cardiovascular surgery2020
Effects of genetic transfection on calcium cycling pathways mediated by double-stranded adeno-associated virus in postinfarction remodeling.
Article in The Journal of thoracic and cardiovascular surgery, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- Progress in the treatment of diabetic cardiomyopathy, a systematic review.Pharmacology research & perspectives · 2024Pooled it
- Cardiac-Targeted AAV5-S100A1 Gene Therapy Protects Against Adverse Remodeling and Contractile Dysfunction in Postischemic Hearts.Circulation. Heart failure · 2025Article
- The multifaceted role of mitochondria in cardiac function: insights and approaches.Cell communication and signaling : CCS · 2024Review
- Acid ceramidase gene therapy ameliorates pulmonary arterial hypertension with right heart dysfunction.Respiratory research · 2023Article
- Biologics and their delivery systems: Trends in myocardial infarction.Advanced drug delivery reviews · 2021Review
- Commentary: Doubling down on adeno-associated viruses for cardiac gene therapy.The Journal of thoracic and cardiovascular surgery · 2020Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveRestoring calcium sensor protein (S100A1) activity in failing hearts poses a promising therapeutic strategy. We hypothesize that cardiac overexpression of the S100A1 gene mediated by a double-stranded adeno-associated virus (scAAV) results in better functional and molecular improvements compared with the single-stranded virus (ssAAV).
methodsHeart failure was induced by coronary artery ligation. Then, intramyocardial injections of saline, AAV9 empty capsid, scAAV9.S100A1, and ssAAV9.S100A1 were performed. Ten weeks postinfarction, all rats received cardiac evaluation; serum and tissue were collected for genetic analysis, cytokine profiling, and assessments of mitochondrial function and structure.
resultsOverexpression of AAV9.S100A1 improved systolic and diastolic function. Compared with control, ejection fraction was greater in treated groups (54.8% vs 32.3%, P < .05). Similarly, end-diastolic volume index was significantly less in the treated group than in control (1.14 vs 1.59 mL/cm
conclusionsGene therapy of S100A1 can prevent pathologic postmyocardial infarction remodeling and decrease inflammatory response in ischemic heart failure.
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Registered trials
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