ReviewComprehensive Physiology2018
Immunobiology of Inherited Muscular Dystrophies.
Review in Comprehensive Physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 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
98 citing papers in PubMed, 160 citations in OpenAlex.
- Proteomic Profiling of Myofiber Repair Annexins and Their Role in Duchenne Muscular Dystrophy.Proteomics · 2026Review
- CTLA4-Ig reduces proliferation and inflammatory gene expression in muscle fibroblasts, corresponding to less fibrosis and inflammation inAmerican journal of physiology. Cell physiology · 2026Article
- Immunohistological and electron microscopy profile of unique TIRM-MRI guided muscle biopsies of FSHD patients.Journal of neuromuscular diseases · 2026Article
- Dystrophins DP71 and DP427 determine cell viability during proliferation and myofibre differentiation.Cell death & disease · 2026Article
- The IL-1β/NETs/AIM2 axis participates in the formation of trauma-induced heterotopic ossification by orchestrating crosstalk between neutrophils and macrophages.Journal of advanced research · 2026Article
- Voluntary running sustains the correction of inflammation-related gene expression conferred by AAV gene therapy in mdx mice.Molecular therapy. Advances · 2026Article
- Direct aldosterone stimulation of skeletal muscle fibroblasts changes gene expression and differentially affects fibroblast functions from normal and diseased muscles.Frontiers in physiology · 2026Article
- Mineralocorticoid receptor antagonists reduce inflammatory signaling independent of myofiber mineralocorticoid receptor.Endocrine and metabolic science · 2025Article
- Tauroursodeoxycholic acid-induced increase in ectopic muscle mineralization occurs exclusively in dystrophic muscles and is independent of endoplasmic reticulum stress.Scientific reports · 2025Article
- Comparative Transcriptomic Profiling in Patients Affected by Duchenne and Becker Muscular Dystrophies: A Focus on ECM Genes Dysregulation.International journal of molecular sciences · 2025Article
- D- and L-Amino Acid Blood Concentrations Are Affected in Children With Duchenne Muscular Dystrophy.Journal of cellular and molecular medicine · 2025Article
- Skeletal muscle disorders as risk factors for type 2 diabetes.Molecular and cellular endocrinology · 2025Review
- Functional Foods, a Hope to Delay Muscle Dystrophy Progression: A Potential Role for Omega Fatty Acids.Nutrients · 2025Review
- Targeting Galectin-3 to modulate inflammation in LAMA2-deficient congenital muscular dystrophy.bioRxiv : the preprint server for biology · 2025Article
- Role of Perinatal Stem Cell Secretome as Potential Therapy for Muscular Dystrophies.Biomedicines · 2025Review
- Review
- Plasmid Gene Therapy for Monogenic Disorders: Challenges and Perspectives.Pharmaceutics · 2025Review
- Respiratory pathology in the mdx/utrn -/- mouse: A murine model for Duchenne Muscular Dystrophy (DMD).PloS one · 2025Article
- Scientific and Technological Prospecting on Polymeric Particles Containing Extracellular Matrix Peptides for the Treatment of Duchenne Muscular Dystrophy.Recent advances in drug delivery and formulation · 2025Review
- Nanomaterial-Mediated Reprogramming of Macrophages to Inhibit Refractory Muscle Fibrosis.Advanced materials (Deerfield Beach, Fla.) · 2024Article
38 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The immune response to acute muscle damage is important for normal repair. However, in chronic diseases such as many muscular dystrophies, the immune response can amplify pathology and play a major role in determining disease severity. Muscular dystrophies are inheritable diseases that vary tremendously in severity, but share the progressive loss of muscle mass and function that can be debilitating and lethal. Mutations in diverse genes cause muscular dystrophy, including genes that encode proteins that maintain membrane strength, participate in membrane repair, or are components of the extracellular matrix or the nuclear envelope. In this article, we explore the hypothesis that an important feature of many muscular dystrophies is an immune response adapted to acute, infrequent muscle damage that is misapplied in the context of chronic injury. We discuss the involvement of the immune system in the most common muscular dystrophy, Duchenne muscular dystrophy, and show that the immune system influences muscle death and fibrosis as disease progresses. We then present information on immune cell function in other muscular dystrophies and show that for many muscular dystrophies, release of cytosolic proteins into the extracellular space may provide an initial signal, leading to an immune response that is typically dominated by macrophages, neutrophils, helper T-lymphocytes, and cytotoxic T-lymphocytes. Although those features are similar in many muscular dystrophies, each muscular dystrophy shows distinguishing features in the magnitude and type of inflammatory response. These differences indicate that there are disease-specific immunomodulatory molecules that determine response to muscle cell damage caused by diverse genetic mutations. © 2018 American Physiological Society. Compr Physiol 8:1313-1356, 2018.
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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.