ReviewFrontiers in immunology2023
Trained immunity as a potential target for therapeutic immunomodulation in Duchenne muscular dystrophy.
Review in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 14 citations in OpenAlex.
- Single nuclei/cell transcriptomics reveal DMD driven cell dynamics and mechanisms of fibroblast inflammatory tissue priming in human dystrophic muscle.Research square · 2026Article
- Early Taurine Administration Decreases the Levels of Receptor-Interacting Serine/Threonine Protein Kinase 1 in the Duchenne Mouse ModelBrain sciences · 2025Article
- Advances in the Regulation by Immune Cells of Skeletal Myositis Outcomes.Aging and disease · 2025Review
- Trained immunity in chronic inflammatory diseases and cancer.Nature reviews. Immunology · 2025Review
- Role of Perinatal Stem Cell Secretome as Potential Therapy for Muscular Dystrophies.Biomedicines · 2025Review
- Macrophage immunometabolism: emerging targets for regrowth in aging muscle.American journal of physiology. Endocrinology and metabolism · 2025Review
- Respiratory pathology in the mdx/utrn -/- mouse: A murine model for Duchenne Muscular Dystrophy (DMD).PloS one · 2025Article
- Advocating the role of trained immunity in the pathogenesis of ME/CFS: a mini review.Frontiers in immunology · 2025Review
- The Role of Pattern Recognition Receptors in Epigenetic and Metabolic Reprogramming: Insights into Trained Immunity.Journal of inflammation research · 2025Review
- Nanomaterial-Mediated Reprogramming of Macrophages to Inhibit Refractory Muscle Fibrosis.Advanced materials (Deerfield Beach, Fla.) · 2024Article
- How Can Proteomics Help to Elucidate the Pathophysiological Crosstalk in Muscular Dystrophy and Associated Multi-System Dysfunction?Proteomes · 2024Article
- The causes and consequences of trained immunity in myeloid cells.Frontiers in immunology · 2024Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Dysregulated inflammation involving innate immune cells, particularly of the monocyte/macrophage lineage, is a key contributor to the pathogenesis of Duchenne muscular dystrophy (DMD). Trained immunity is an evolutionarily ancient protective mechanism against infection, in which epigenetic and metabolic alterations confer non-specific hyperresponsiveness of innate immune cells to various stimuli. Recent work in an animal model of DMD (mdx mice) has shown that macrophages exhibit cardinal features of trained immunity, including the presence of innate immune system "memory". The latter is reflected by epigenetic changes and durable transmissibility of the trained phenotype to healthy non-dystrophic mice by bone marrow transplantation. Mechanistically, it is suggested that a Toll-like receptor (TLR) 4-regulated, memory-like capacity of innate immunity is induced at the level of the bone marrow by factors released from the damaged muscles, leading to exaggerated upregulation of both pro- and anti-inflammatory genes. Here we propose a conceptual framework for the involvement of trained immunity in DMD pathogenesis and its potential to serve as a new therapeutic target.
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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 Socratic graph.