ArticleJCI insight2023
Cardiac gene therapy treats diabetic cardiomyopathy and lowers blood glucose.
Article in JCI insight, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 2 of them syntheses 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.
The trial behind it
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
16 citing papers in PubMed, 2 syntheses or guidelines pooled it, 27 citations in OpenAlex.
- Cardiac energy substrate utilization in heart failure with preserved ejection fraction: reconciling conflicting evidence on fatty acid and glucose metabolism.American journal of physiology. Heart and circulatory physiology · 2025Pooled it
- Progress in the treatment of diabetic cardiomyopathy, a systematic review.Pharmacology research & perspectives · 2024Pooled it
- Myocardial PKG1α dysregulation contributes to ventricular tachycardia pathogenesis in type 2 diabetes and metabolic syndrome.Heart rhythm · 2026Article
- Calcium dysregulation in diabetic cardiomyopathy & heart failure with preserved ejection fraction.Frontiers in cardiovascular medicine · 2026Review
- Cardiac Cell Remodeling in Obesity and Diabetes.Handbook of experimental pharmacology · 2026Review
- Diagnostic significance of cardiac bridging integrator 1 score in hospitalized patients with heart failure with preserved ejection fraction and its assessment of prognostic value for major adverse cardiac events.BMC cardiovascular disorders · 2025Article
- BIN1 gene replacement reverses BIN1-related centronuclear myopathy.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- AAV9-cBIN1 gene therapy rescues chronic heart failure due to ischemic cardiomyopathy in a canine model.Communications medicine · 2025Article
- Restoration of Sestrin 3 Expression Mitigates Cardiac Oxidative Damage in Ischemia-Reperfusion Injury Model.Antioxidants (Basel, Switzerland) · 2025Article
- Assessment of serum caveolin-3 levels in patients with heart failure.Frontiers in cardiovascular medicine · 2025Article
- AAV viral vectors as therapeutic interventions for inherited or non-inherited cardiac disorders: current aspects and future prospects.Frontiers in medicine · 2025Review
- Mechanistic Relevance of Ventricular Arrhythmias in Heart Failure with Preserved Ejection Fraction.International journal of molecular sciences · 2024Review
- Cardiac bridging integrator 1 gene therapy rescues chronic non-ischemic heart failure in minipigs.NPJ Regenerative medicine · 2024Article
- Enhanced CaJACC. Clinical electrophysiology · 2024Article
- Roles of distinct nuclear receptors in diabetic cardiomyopathy.Frontiers in pharmacology · 2024Review
- Effects of scutellarin on the mechanism of cardiovascular diseases: a review.Frontiers in pharmacology · 2023Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 4 countries.
Funding
Abstract
Diabetic cardiomyopathy, an increasingly global epidemic and a major cause of heart failure with preserved ejection fraction (HFpEF), is associated with hyperglycemia, insulin resistance, and intracardiomyocyte calcium mishandling. Here we identify that, in db/db mice with type 2 diabetes-induced HFpEF, abnormal remodeling of cardiomyocyte transverse-tubule microdomains occurs with downregulation of the membrane scaffolding protein cardiac bridging integrator 1 (cBIN1). Transduction of cBIN1 by AAV9 gene therapy can restore transverse-tubule microdomains to normalize intracellular distribution of calcium-handling proteins and, surprisingly, glucose transporter 4 (GLUT4). Cardiac proteomics revealed that AAV9-cBIN1 normalized components of calcium handling and GLUT4 translocation machineries. Functional studies further identified that AAV9-cBIN1 normalized insulin-dependent glucose uptake in diabetic cardiomyocytes. Phenotypically, AAV9-cBIN1 rescued cardiac lusitropy, improved exercise intolerance, and ameliorated hyperglycemia in diabetic mice. Restoration of transverse-tubule microdomains can improve cardiac function in the setting of diabetic cardiomyopathy and can also improve systemic glycemic control.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.