ArticleJournal of molecular and cellular cardiology2014
Dystrobrevin increases dystrophin's binding to the dystrophin-glycoprotein complex and provides protection during cardiac stress.
Article in Journal of molecular and cellular cardiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 30 citations in OpenAlex.
- DG9 boosts PMO nuclear uptake and exon skipping to restore dystrophic muscle and cardiac function.Nature communications · 2025Article
- Functional cardiac consequences of β-adrenergic stress-induced injury in a model of Duchenne muscular dystrophy.Disease models & mechanisms · 2024Article
- Reduced cardiac antioxidant defenses mediate increased susceptibility to workload-induced myocardial injury in males with genetic cardiomyopathy.Journal of molecular and cellular cardiology · 2024Article
- Functional cardiac consequences of β-adrenergic stress-induced injury in thebioRxiv : the preprint server for biology · 2024Article
- Dystrophin- and Utrophin-Based Therapeutic Approaches for Treatment of Duchenne Muscular Dystrophy: A Comparative Review.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2024Review
- A microtubule-connexin-43 regulatory link suppresses arrhythmias and cardiac fibrosis in Duchenne muscular dystrophy mice.American journal of physiology. Heart and circulatory physiology · 2022Article
- Cmarr/miR-540-3p axis promotes cardiomyocyte maturation transition by orchestrating Dtna expression.Molecular therapy. Nucleic acids · 2022Article
- AFrontiers in cell and developmental biology · 2022Article
- DMD carrier model with mosaic dystrophin expression in the heart reveals complex vulnerability to myocardial injury.Human molecular genetics · 2020Article
- Cardiac Pathophysiology and the Future of Cardiac Therapies in Duchenne Muscular Dystrophy.International journal of molecular sciences · 2019Review
- Acute ATJournal of molecular and cellular cardiology · 2019Article
- Mice lacking α-, β1- and β2-syntrophins exhibit diminished function and reduced dystrophin expression in both cardiac and skeletal muscle.Human molecular genetics · 2019Article
- CRABP1 protects the heart from isoproterenol-induced acute and chronic remodeling.The Journal of endocrinology · 2018Article
- Humanizing the mdx mouse model of DMD: the long and the short of it.NPJ Regenerative medicine · 2018Review
- Measuring Pressure Volume Loops in the Mouse.Journal of visualized experiments : JoVE · 2016Article
- Microtubule-Mediated Misregulation of Junctophilin-2 Underlies T-Tubule Disruptions and Calcium Mishandling inJACC. Basic to translational science · 2016Article
- Hypoxia-induced cardiac injury in dystrophic mice.American journal of physiology. Heart and circulatory physiology · 2016Article
- Ring chromosome 18 in combination with 18q12.1 (DTNA) interstitial microdeletion in a patient with multiple congenital defects.Molecular cytogenetics · 2016Article
- Combinatorial therapeutic activation with heparin and AICAR stimulates additive effects on utrophin A expression in dystrophic muscles.Human molecular genetics · 2016Article
- Diastolic dysfunction precedes hypoxia-induced mortality in dystrophic mice.Physiological reports · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Duchenne muscular dystrophy is a fatal progressive disease of both cardiac and skeletal muscle resulting from the mutations in the DMD gene and loss of the protein dystrophin. Alpha-dystrobrevin (α-DB) tightly associates with dystrophin but the significance of this interaction within cardiac myocytes is poorly understood. In the current study, the functional role of α-DB in cardiomyocytes and its implications for dystrophin function are examined. Cardiac stress testing demonstrated significant heart disease in α-DB null (adbn(-/-)) mice, which displayed mortality and lesion sizes that were equivalent to those seen in dystrophin-deficient mdx mice. Despite normal expression and subcellular localization of dystrophin in the adbn(-/-) heart, there is a significant decrease in the strength of dystrophin's interaction with the membrane-bound dystrophin-associated glycoprotein complex (DGC). A similar weakening of the dystrophin-membrane interface was observed in mice lacking the sarcoglycan complex. Cardiomyocytes from adbn(-/-) mice were smaller and responded less to adrenergic receptor induced hypertrophy. The basal decrease in size could not be attributed to aberrant Akt activation. In addition, the organization of the microtubule network was significantly altered in adbn(-/-) cardiac myocytes, while the total expression of tubulin was unchanged in adbn(-/-) hearts. These studies demonstrate that α-DB is a multifunctional protein that increases dystrophin's binding to the dystrophin-glycoprotein complex, and is critical for the full functionality of dystrophin.
Indexed as
Identifiers
What OpenQuestion holds
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.