ArticleRare diseases (Austin, Tex.)2015
The immune system in Duchenne muscular dystrophy: Friend or foe.
Article in Rare diseases (Austin, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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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Who cites it
44 citing papers in PubMed, 76 citations in OpenAlex.
- Transcriptome analysis of injured muscle identifies new candidate genes for satellite cell growth and myofiber formation during early muscle regeneration.Animal bioscience · 2026Article
- Inhibition of HuR/ELAVL-1 attenuates fibrotic progression in Mdx mice with dilated cardiomyopathy.Cellular and molecular life sciences : CMLS · 2025Article
- Bidirectional role of Costameres in the pathophysiology of mdx skeletal muscles.Human molecular genetics · 2025Article
- Immunoproteasome Inhibition Positively Impacts the Gut-Muscle Axis in Duchenne Muscular Dystrophy.Journal of cachexia, sarcopenia and muscle · 2025Article
- The curious case of AAV immunology.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Functional Foods, a Hope to Delay Muscle Dystrophy Progression: A Potential Role for Omega Fatty Acids.Nutrients · 2025Review
- Benfotiamine improves dystrophic pathology and exercise capacity in mdx mice by reducing inflammation and fibrosis.Human molecular genetics · 2024Article
- How Can Proteomics Help to Elucidate the Pathophysiological Crosstalk in Muscular Dystrophy and Associated Multi-System Dysfunction?Proteomes · 2024Article
- Article
- Association between blood eosinophil count and Duchenne muscular dystrophy severity and prognosis: a retrospective cohort study.Italian journal of pediatrics · 2023Article
- Duchenne muscular dystrophy: disease mechanism and therapeutic strategies.Frontiers in physiology · 2023Review
- Immunoproteasome Inhibition Ameliorates Aged Dystrophic Mouse Muscle Environment.International journal of molecular sciences · 2022Article
- Next-Generation SINE Compound KPT-8602 Ameliorates Dystrophic Pathology in Zebrafish and Mouse Models of DMD.Biomedicines · 2022Article
- Regulatory T cells-centered regulatory networks of skeletal muscle inflammation and regeneration.Cell & bioscience · 2022Review
- Selective ablation of Nfix in macrophages attenuates muscular dystrophy by inhibiting fibro-adipogenic progenitor-dependent fibrosis.The Journal of pathology · 2022Article
- Inhibition of PKCθ Improves Dystrophic Heart Phenotype and Function in a Novel Model of DMD Cardiomyopathy.International journal of molecular sciences · 2022Article
- P2X7 Receptor Antagonist Reduces Fibrosis and Inflammation in a Mouse Model of Alpha-Sarcoglycan Muscular Dystrophy.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Treating Duchenne Muscular Dystrophy: The Promise of Stem Cells, Artificial Intelligence, and Multi-Omics.Frontiers in cardiovascular medicine · 2022Review
- The Immune System in Duchenne Muscular Dystrophy Pathogenesis.Biomedicines · 2021Review
- The Interplay of Mitophagy and Inflammation in Duchenne Muscular Dystrophy.Life (Basel, Switzerland) · 2021Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Duchenne muscular dystrophy (DMD) is a genetic disease caused by mutations in the X-linked dystrophin gene, resulting in reduced or absent protein production, subsequently leading to the structural instability of the dystroglycan complex (DGC), muscle degeneration, and early death in males. Thus, current treatments have been targeting the genetic defect either by bypassing the mutation through exon skipping or replacing the defective gene through gene therapy and stem cell approaches. However, what has been an underappreciated mediator of muscle pathology and, ultimately, of muscle degeneration and fibrotic replacement, is the prominent inflammatory response. Of potentially critical importance, however, is the fact that the elements mediating the inflammatory response also play an essential role in tissue repair. In this opinion piece, we highlight the detrimental and supportive immune parameters that occur as a consequence of the genetic disorder and discuss how changes to immunity can potentially ameliorate the disease intensity and be employed in conjunction with efforts to correct the genetic disorder.
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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.