ArticleHuman molecular genetics2019
Embryonic myosin is a regeneration marker to monitor utrophin-based therapies for DMD.
Article in Human molecular genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 38 citations in OpenAlex.
- Exploring Dystrophin Expression and Mutations in theInternational journal of molecular sciences · 2026Article
- ANXA11 suppression restores muscular function in the mdx mouse model of Duchenne muscular dystrophy (DMD).Nature communications · 2026Article
- Voluntary running sustains the correction of inflammation-related gene expression conferred by AAV gene therapy in mdx mice.Molecular therapy. Advances · 2026Article
- (Z)-Endoxifen as a Potential Modulator of Utrophin Pathways in Duchenne Muscular Dystrophy: A Mechanistic and Transcriptomic Perspective.Degenerative neurological and neuromuscular disease · 2026Review
- Effect of analgesic treatments on voluntary activity, mechanical sensitivity and muscle regeneration after cardiotoxin injection in mice.Scientific reports · 2025Article
- Myoblast-derived ADAMTS-like 2 promotes skeletal muscle regeneration after injury.NPJ Regenerative medicine · 2024Article
- Satellite cell-derived TRIM28 is pivotal for mechanical load- and injury-induced myogenesis.EMBO reports · 2024Article
- A Novel Minimally Invasive Surgically Induced Skeletal Muscle Injury Model in Sheep.International journal of molecular sciences · 2024Article
- NLRP3 Contributes to Sarcopenia Associated to Dependency Recapitulating Inflammatory-Associated Muscle Degeneration.International journal of molecular sciences · 2024Article
- Achieving myoblast engraftment into intact skeletal muscle via extracellular matrix.Frontiers in cell and developmental biology · 2024Article
- Indian Ornamental Tarantula (Cells · 2023Article
- Systemic deletion ofProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Histological Methods to Assess Skeletal Muscle Degeneration and Regeneration in Duchenne Muscular Dystrophy.International journal of molecular sciences · 2022Review
- Construction of Plasmid DNA Expressing Two Isoforms of Insulin-Like Growth Factor-1 and Its Effects on Skeletal Muscle Injury Models.Human gene therapy · 2022Article
- The skeletal muscle phenotype of the DE50-MD dog model of Duchenne muscular dystrophy.Wellcome open research · 2022Article
- Loss of sarcospan exacerbates pathology in mdx mice, but does not affect utrophin amelioration of disease.Human molecular genetics · 2021Article
- Twenty-one days of low-intensity eccentric training improve morphological characteristics and function of soleus muscles of mdx mice.Scientific reports · 2021Article
- The administration of antisense oligonucleotide golodirsen reduces pathological regeneration in patients with Duchenne muscular dystrophy.Acta neuropathologica communications · 2021Article
- Review
- Lack of miR-378 attenuates muscular dystrophy in mdx mice.JCI insight · 2020Article
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 1 institution in 1 country.
Funding
Abstract
Duchenne muscular dystrophy (DMD) is a lethal, X-linked muscle-wasting disease caused by lack of the cytoskeletal protein dystrophin. Constitutive utrophin expression, a structural and functional paralogue of dystrophin, can successfully prevent the dystrophic pathology in the dystrophin-deficient mdx mouse model. In dystrophic muscles, utrophin is increased as part of the repair process and localized at the sarcolemma of regenerating myofibers. The presence of developmental myosin such as embryonic myosin (MyHC-emb) and neonatal represents a useful marker of muscle regeneration and a meaningful indicator of muscle damage, which correlates with the clinical severity of milder Becker muscular dystrophy and DMD patients. In the present study, we demonstrate that MyHC-emb is a robust marker of regeneration at different ages and in different skeletal muscles. We also evaluate the correlation between utrophin, dystrophin and MyHC-emb in wild-type (wt) and regenerating dystrophic muscles. Restoration of dystrophin significantly reduced MyHC-emb levels. Similarly, overexpression of utrophin in the transgenic mdx-Fiona mice reduced the number of MyHC-emb positive fibers to wt level, prevented the regenerative process and rescued the muscle function. In contrast, the absence of utrophin in the dystrophin-deficient double-knockout mice resulted in a higher MyHC-emb content and in a more severe dystrophic pathophysiology than in mdx mice. These data illustrate the importance of monitoring utrophin and MyHC-emb levels in the preclinical evaluation of therapies and provide translational support for the use of developmental myosin as a disease biomarker in DMD clinical trials.
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.