ArticleAmerican journal of physiology. Cell physiology2010
Extensive mononuclear infiltration and myogenesis characterize recovery of dysferlin-null skeletal muscle from contraction-induced injuries.
Article in American journal of physiology. Cell physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 47 papers, 1 of them a synthesis 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.
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Who cites it
47 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.
- Minimal Evidence for a Secondary Loss of Strength After an Acute Muscle Injury: A Systematic Review and Meta-Analysis.Sports medicine (Auckland, N.Z.) · 2017Pooled it
- Excess muscle plasma membrane leak disrupts ECM content and shifts macrophage-mediated muscle repair.JCI insight · 2026Article
- Dysferlin and the Regulation of CaCells · 2025Review
- Bioengineered Model of Human LGMD2B Skeletal Muscle Reveals Roles of Intracellular Calcium Overload in Contractile and Metabolic Dysfunction in Dysferlinopathy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Role of calcium-sensor proteins in cell membrane repair.Bioscience reports · 2023Review
- Dosage-Adjusted Resistance Training in Mice with a Reduced Risk of Muscle Damage.Journal of visualized experiments : JoVE · 2022Article
- The C2 domains of dysferlin: roles in membrane localization, CaThe Journal of physiology · 2022Article
- Elevated CaFrontiers in physiology · 2022Article
- Minimally Invasive Muscle Embedding Generates Donor-Cell-Derived Muscle Fibers that Express Desmin and Dystrophin.Military medicine · 2020Article
- Keratin 18 is an integral part of the intermediate filament network in murine skeletal muscle.American journal of physiology. Cell physiology · 2020Article
- Engineered skeletal muscles for disease modeling and drug discovery.Biomaterials · 2019Review
- Muscle xenografts reproduce key molecular features of facioscapulohumeral muscular dystrophy.Experimental neurology · 2019Article
- Massage increases satellite cell number independent of the age-associated alterations in sarcolemma permeability.Physiological reports · 2019Article
- Faster regeneration associated to high expression of Fam65b and Hdac6 in dysferlin-deficient mouse.Journal of molecular histology · 2019Article
- Dysferlin-deficiency has greater impact on function of slow muscles, compared with fast, in aged BLAJ mice.PloS one · 2019Article
- Identification of Novel Antisense-Mediated Exon Skipping Targets in DYSF for Therapeutic Treatment of Dysferlinopathy.Molecular therapy. Nucleic acids · 2018Article
- Can obesity-induced inflammation in skeletal muscle and intramuscular adipose tissue accurately detect liver fibrosis?Journal of musculoskeletal & neuronal interactions · 2018Article
- Immunobiology of Inherited Muscular Dystrophies.Comprehensive Physiology · 2018Review
- Diltiazem improves contractile properties of skeletal muscle in dysferlin-deficient BLAJ mice, but does not reduce contraction-induced muscle damage.Physiological reports · 2018Article
- Effect of Ibuprofen on Skeletal Muscle of Dysferlin-Null Mice.The Journal of pharmacology and experimental therapeutics · 2018Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
We studied the response of dysferlin-null and control skeletal muscle to large- and small-strain injuries to the ankle dorsiflexors in mice. We measured contractile torque and counted fibers retaining 10-kDa fluorescein dextran, necrotic fibers, macrophages, and fibers with central nuclei and expressing developmental myosin heavy chain to assess contractile function, membrane resealing, necrosis, inflammation, and myogenesis. We also studied recovery after blunting myogenesis with X-irradiation. We report that dysferlin-null myofibers retain 10-kDa dextran for 3 days after large-strain injury but are lost thereafter, following necrosis and inflammation. Recovery of dysferlin-null muscle requires myogenesis, which delays the return of contractile function compared with controls, which recover from large-strain injury by repairing damaged myofibers without significant inflammation, necrosis, or myogenesis. Recovery of control and dysferlin-null muscles from small-strain injury involved inflammation and necrosis followed by myogenesis, all of which were more pronounced in the dysferlin-null muscles, which recovered more slowly. Both control and dysferlin-null muscles also retained 10-kDa dextran for 3 days after small-strain injury. We conclude that dysferlin-null myofibers can survive contraction-induced injury for at least 3 days but are subsequently eliminated by necrosis and inflammation. Myogenesis to replace lost fibers does not appear to be significantly compromised in dysferlin-null mice.
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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.