ArticleThe Journal of physiology2016
Eliminating Nox2 reactive oxygen species production protects dystrophic skeletal muscle from pathological calcium influx assessed in vivo by manganese-enhanced magnetic resonance imaging.
Article in The Journal of physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- Using MRI to quantify skeletal muscle pathology in Duchenne muscular dystrophy: A systematic mapping review.Muscle & nerve · 2021Pooled it
- Differentiated skeletal myotubes coupled with bimodal biosensing for dynamic functional evaluation of inflammatory myotube dysfunction.Microsystems & nanoengineering · 2026Article
- Manganese-Enhanced Magnetic Resonance Imaging: From Translational Research to First-in-Human Trials in Oncology.Molecular diagnosis & therapy · 2026Review
- Acute microtubule changes linked to DMD pathology are insufficient to impair contractile function or enhance contraction-induced injury in healthy muscle.bioRxiv : the preprint server for biology · 2024Article
- Modulation of sarcopenia phenotypes by glutathione peroxidase 4 overexpression in mice.The Journal of physiology · 2023Article
- Protection of dystrophic muscle cells using Idebenone correlates with the interplay between calcium, oxidative stress and inflammation.International journal of experimental pathology · 2023Article
- A deep redox proteome profiling workflow and its application to skeletal muscle of a Duchenne Muscular Dystrophy model.Free radical biology & medicine · 2022Article
- NOX4 inhibition promotes the remodeling of dystrophic muscle.JCI insight · 2022Article
- Targeting Nrf2 for the treatment of Duchenne Muscular Dystrophy.Redox biology · 2021Review
- Abnormal Calcium Handling in Duchenne Muscular Dystrophy: Mechanisms and Potential Therapies.Frontiers in physiology · 2021Review
- Molecular changes in transcription and metabolic pathways underlying muscle atrophy in the CuZnSOD null mouse model of sarcopenia.GeroScience · 2020Article
- Mechanical factors tune the sensitivity of mdx muscle to eccentric strength loss and its protection by antioxidant and calcium modulators.Skeletal muscle · 2020Article
- The Emerging Roles of Nicotinamide Adenine Dinucleotide Phosphate Oxidase 2 in Skeletal Muscle Redox Signaling and Metabolism.Antioxidants & redox signaling · 2019Review
- Coenzyme Q10 supplementation acts as antioxidant on dystrophic muscle cells.Cell stress & chaperones · 2019Article
- Summary of Imaging in 2020: Visualizing the Future of Healthcare with MR Imaging.Molecular imaging and biology · 2019Article
- Xanthine oxidase is hyper-active in Duchenne muscular dystrophy.Free radical biology & medicine · 2018Article
- Loss of peroxiredoxin-2 exacerbates eccentric contraction-induced force loss in dystrophin-deficient muscle.Nature communications · 2018Article
- Neopterin/7,8-dihydroneopterin is elevated in Duchenne muscular dystrophy patients and protects mdx skeletal muscle function.Experimental physiology · 2018Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
key pointsInhibiting Nox2 reactive oxygen species (ROS) production reduced in vivo calcium influx in dystrophic muscle. The lack of Nox2 ROS production protected against decreased in vivo muscle function in dystrophic mice. Manganese-enhanced magnetic resonance imaging (MEMRI) was able to detect alterations in basal calcium levels in skeletal muscle and differentiate disease status. Administration of Mn ABSTRACT: Duchenne muscular dystrophy (DMD) is an X-linked progressive degenerative disease resulting from a mutation in the gene that encodes dystrophin, leading to decreased muscle mechanical stability and force production. Increased Nox2 reactive oxygen species (ROS) production and sarcolemmal Ca
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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.