ArticleJournal of cellular and molecular medicine2012
The heart in Duchenne muscular dystrophy: early detection of contractile performance alteration.
Article in Journal of cellular and molecular medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 17 citations in OpenAlex.
- Fighting for every beat: cardiac therapies in Duchenne muscular dystrophy.Skeletal muscle · 2025Review
- Review
- Preservation of shortening velocity and power output in single muscle fibres from patients with idiopathic inflammatory myopathies.Journal of muscle research and cell motility · 2023Article
- Two-dimensional speckle tracking echocardiography demonstrates improved myocardial function after intravenous infusion of bone marrow mesenchymal stem in the X-Linked muscular dystrophy mice.BMC cardiovascular disorders · 2022Article
- Natural History of Histopathologic Changes in Cardiomyopathy of Golden Retriever Muscular Dystrophy.Frontiers in veterinary science · 2021Article
- Identification of a myotropic AAV by massively parallel in vivo evaluation of barcoded capsid variants.Nature communications · 2020Article
- Left Ventricular Tonic Contraction as a Novel Biomarker of Cardiomyopathy in Duchenne Muscular Dystrophy.Pediatric cardiology · 2016Article
- Proteomic profiling of the dystrophin-deficient mdx phenocopy of dystrophinopathy-associated cardiomyopathy.BioMed research international · 2014Review
- Hierarchical accumulation of RyR post-translational modifications drives disease progression in dystrophic cardiomyopathy.Cardiovascular research · 2013Article
- Full-length dystrophin deficiency leads to contractile and calcium transient defects in human engineered heart tissues.Journal of tissue engineeringArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Progressive cardiomyopathy is a major cause of death in Duchenne muscular dystrophy (DMD) patients. Coupling between Ca(2+) handling and contractile properties in dystrophic hearts is poorly understood. It is also not clear whether developing cardiac failure is dominated by alterations in Ca(2+) pathways or more related to the contractile apparatus. We simultaneously recorded force and Ca(2+) transients in field-stimulated papillary muscles from young (10-14 weeks) wild-type (wt) and dystrophic mdx mice. Force amplitudes were fivefold reduced in mdx muscles despite only 30% reduction in fura-2 ratio amplitudes. This indicated mechanisms other than systolic Ca(2+) to additionally account for force decrements in mdx muscles. pCa-force relations revealed decreased mdx myofibrillar Ca(2+) sensitivity. 'In vitro' motility assays, studied in mdx hearts here for the first time, showed significantly slower sliding velocities. mdx MLC/MHC isoforms were not grossly altered. Dystrophic hearts showed echocardiography signs of early ventricular wall hypertrophy with a significantly enlarged end-diastolic diameter 'in vivo'. However, fractional shortening was still comparable to wt mice. Changes in the contractile apparatus satisfactorily explained force drop in mdx hearts. We give first evidence of early hypertrophy in mdx mice and possible mechanisms for already functional impairment of cardiac muscle in DMD.
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.