ArticleHuman molecular genetics2014
Eccentric muscle challenge shows osteopontin polymorphism modulation of muscle damage.
Article in Human molecular genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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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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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.
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- Bone-derived factors mediate crosstalk between skeletal and extra-skeletal organs.Bone research · 2025Review
- The complex landscape of DMD mutations: moving towards personalized medicine.Frontiers in genetics · 2024Review
- Is it time for genetic modifiers to predict prognosis in Duchenne muscular dystrophy?Nature reviews. Neurology · 2023Review
- Development of outcome measures according to dystrophic phenotypes in canine X-linked muscular dystrophy in Japan.Experimental animals · 2021Article
- Genetic Modifiers and Phenotype of Duchenne Muscular Dystrophy: A Systematic Review and Meta-Analysis.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Genetic Modifiers of Duchenne Muscular Dystrophy in Chinese Patients.Frontiers in neurology · 2020Article
- The "Usual Suspects": Genes for Inflammation, Fibrosis, Regeneration, and Muscle Strength Modify Duchenne Muscular Dystrophy.Journal of clinical medicine · 2019Review
- Changes in Muscle Metabolism are Associated with Phenotypic Variability in Golden Retriever Muscular Dystrophy.The Yale journal of biology and medicine · 2017Article
- Changes in muscle fiber contractility and extracellular matrix production during skeletal muscle hypertrophy.Journal of applied physiology (Bethesda, Md. : 1985) · 2017Article
- Outside in: The matrix as a modifier of muscular dystrophy.Biochimica et biophysica acta. Molecular cell research · 2017Review
- OPN-a induces muscle inflammation by increasing recruitment and activation of pro-inflammatory macrophages.Experimental physiology · 2016Article
- Genetic variation and exercise-induced muscle damage: implications for athletic performance, injury and ageing.European journal of applied physiology · 2016Review
- Anti-inflammatory drugs for Duchenne muscular dystrophy: focus on skeletal muscle-releasing factors.Drug design, development and therapy · 2016Review
- Genetic modifiers of ambulation in the Cooperative International Neuromuscular Research Group Duchenne Natural History Study.Annals of neurology · 2015Article
- Article
- Exploration of New Contrasts, Targets, and MR Imaging and Spectroscopy Techniques for Neuromuscular Disease - A Workshop Report of Working Group 3 of the Biomedicine and Molecular Biosciences COST Action BM1304 MYO-MRI.Journal of neuromuscular diseasesArticle
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
A promoter polymorphism of the osteopontin (OPN) gene (rs28357094) has been associated with multiple inflammatory states, severity of Duchenne muscular dystrophy (DMD) and muscle size in healthy young adults. We sought to define the mechanism of action of the polymorphism, using allele-specific in vitro reporter assays in muscle cells, and a genotype-stratified intervention in healthy controls. In vitro reporter constructs showed the G allele to respond to estrogen treatment, whereas the T allele showed no transcriptional response. Young adult volunteers (n = 187) were enrolled into a baseline study, and subjects with specific rs28357094 genotypes enrolled into an eccentric muscle challenge intervention [n = 3 TT; n = 3 GG/GT (dominant inheritance model)]. Female volunteers carrying the G allele showed significantly greater inflammation and increased muscle volume change as determined by magnetic resonance imaging T1- and T2-weighted images after eccentric challenge, as well as greater decrement in biceps muscle force. Our data suggest a model where the G allele enables enhanced activities of upstream enhancer elements due to loss of Sp1 binding at the polymorphic site. This results in significantly greater expression of the pro-inflammatory OPN cytokine during tissue remodeling in response to challenge in G allele carriers, promoting muscle hypertrophy in normal females, but increased damage in DMD patients.
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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.