ArticleJournal of applied physiology (Bethesda, Md. : 1985)2017
Altered nuclear dynamics in MDX myofibers.
Article in Journal of applied physiology (Bethesda, Md. : 1985), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 32 citations in OpenAlex.
- The nucleus as a mechanobiological hub in muscle aging.Nucleus (Austin, Tex.) · 2026Review
- NuMA1 controls myonuclear motility in striated skeletal muscle through AMPK activity and is impaired in Duchenne muscular dystrophy.Cell death & disease · 2026Article
- AAVcc47-The Yale journal of biology and medicine · 2026Article
- PPMO-based exon skipping therapy improves respiratory function in theMolecular therapy. Nucleic acids · 2026Article
- Twisting Paths: The Paradox of Fiber Branching in Muscle Regeneration.International journal of molecular sciences · 2026Review
- Interplay between microtubule interactome, myonuclei mechanotransduction, and positioning in myopathies.Nucleus (Austin, Tex.) · 2025Review
- Transcriptomic profiling of skeletal muscle in the DMDScientific reports · 2025Article
- mRNA in situ hybridization exhibits unbalanced nuclear/cytoplasmic dystrophin transcript repartition in Duchenne myogenic cells and skeletal muscle biopsies.Scientific reports · 2023Article
- Dystrophin myonuclear domain restoration governs treatment efficacy in dystrophic muscle.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Detyrosinated microtubule arrays drive myofibrillar malformations inFrontiers in cell and developmental biology · 2023Article
- Nuclear movement in multinucleated cells.Development (Cambridge, England) · 2022Review
- The role of the dystrophin glycoprotein complex in muscle cell mechanotransduction.Communications biology · 2022Review
- Absence of the Z-disc protein α-actinin-3 impairs the mechanical stability of Actn3KO mouse fast-twitch muscle fibres without altering their contractile properties or twitch kinetics.Skeletal muscle · 2022Article
- Lifespan Analysis of DystrophicFrontiers in physiology · 2021Article
- The Nucleoskeleton: Crossroad of Mechanotransduction in Skeletal Muscle.Frontiers in physiology · 2021Review
- Lifetime analysis of mdx skeletal muscle reveals a progressive pathology that leads to myofiber loss.Scientific reports · 2020Article
- Differential YAP nuclear signaling in healthy and dystrophic skeletal muscle.American journal of physiology. Cell physiology · 2019Article
- Misplaced Golgi Elements Produce Randomly Oriented Microtubules and Aberrant Cortical Arrays of Microtubules in Dystrophic Skeletal Muscle Fibers.Frontiers in cell and developmental biology · 2019Article
- NADPH oxidase mediates microtubule alterations and diaphragm dysfunction in dystrophic mice.eLife · 2018Article
- Specialized Positioning of Myonuclei Near Cell-Cell Junctions.Frontiers in physiology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Duchenne muscular dystrophy (DMD) is a genetic disorder in which the absence of dystrophin leads to progressive muscle degeneration and weakness. Although the genetic basis is known, the pathophysiology of dystrophic skeletal muscle remains unclear. We examined nuclear movement in wild-type (WT) and muscular dystrophy mouse model for DMD (MDX) (dystrophin-null) mouse myofibers. We also examined expression of proteins in the linkers of nucleoskeleton and cytoskeleton (LINC) complex, as well as nuclear transcriptional activity via histone H3 acetylation and polyadenylate-binding nuclear protein-1. Because movement of nuclei is not only LINC dependent but also microtubule dependent, we analyzed microtubule density and organization in WT and MDX myofibers, including the application of a unique 3D tool to assess microtubule core structure. Nuclei in MDX myofibers were more mobile than in WT myofibers for both distance traveled and velocity. MDX muscle shows reduced expression and labeling intensity of nesprin-1, a LINC protein that attaches the nucleus to the microtubule and actin cytoskeleton. MDX nuclei also showed altered transcriptional activity. Previous studies established that microtubule structure at the cortex is disrupted in MDX myofibers; our analyses extend these findings by showing that microtubule structure in the core is also disrupted. In addition, we studied malformed MDX myofibers to better understand the role of altered myofiber morphology vs. microtubule architecture in the underlying susceptibility to injury seen in dystrophic muscles. We incorporated morphological and microtubule architectural concepts into a simplified finite element mathematical model of myofiber mechanics, which suggests a greater contribution of myofiber morphology than microtubule structure to muscle biomechanical performance.
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.