ArticleJCI insight2020
Splenic Ly6Chi monocytes are critical players in dystrophic muscle injury and repair.
Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 65 citations in OpenAlex.
- FAP-derived CCL2 is required for adequate monocyte/macrophage infiltration to support acute skeletal muscle injury repair.iScience · 2026Article
- Inflammation in a severe model of dystrophic cardiomyopathy contains a high proportion of T cells that contribute to onset of pathology.American journal of physiology. Heart and circulatory physiology · 2026Article
- Macrophage Infiltration, Activation, and Therapeutic Implication in Skeletal Muscle Injury and Repair.International journal of molecular sciences · 2026Review
- Exercise-Activated Mesenchymal Stem Cells: A Translational Strategy for Age-Related Sarcopenia Management.Stem cell reviews and reports · 2025Review
- Profiles of Monocyte Subsets and Fibrosis-Related Genes in Patients with Muscular Dystrophy Undergoing Intermittent Prednisone Therapy.International journal of molecular sciences · 2025Article
- Organ Crosstalk: The Role of Spleen.Phenomics (Cham, Switzerland) · 2025Review
- Rebalancing Immune Interactions within the Brain-Spleen Axis Mitigates Neuroinflammation in an Aging Mouse Model of Alzheimer's Disease.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- ProBDNF as a Myokine in Skeletal Muscle Injury: Role in Inflammation and Potential for Therapeutic Modulation of p75International journal of molecular sciences · 2025Article
- Macrophages in the Context of Muscle Regeneration and Duchenne Muscular Dystrophy.International journal of molecular sciences · 2024Review
- Effect of epicatechin consumption on the inflammatory pathway and mitochondria morphology in PBMC from a R350P desminopathy patient: A case report.Physiological reports · 2024Article
- Restoring Mitochondrial Function and Muscle Satellite Cell Signaling: Remedies against Age-Related Sarcopenia.Biomolecules · 2024Review
- How Can Proteomics Help to Elucidate the Pathophysiological Crosstalk in Muscular Dystrophy and Associated Multi-System Dysfunction?Proteomes · 2024Article
- Cellular interactions and microenvironment dynamics in skeletal muscle regeneration and disease.Frontiers in cell and developmental biology · 2024Review
- Article
- Cellular pathogenesis of Duchenne muscular dystrophy: progressive myofibre degeneration, chronic inflammation, reactive myofibrosis and satellite cell dysfunction.European journal of translational myology · 2023Article
- Injury-experienced satellite cells retain long-term enhanced regenerative capacity.Stem cell research & therapy · 2023Article
- Sympathetic Nerves Coordinate Corneal Epithelial Wound Healing by Controlling the Mobilization of Ly6Chi Monocytes From the Spleen to the Injured Cornea.Investigative ophthalmology & visual science · 2023Article
- Central and peripheral myeloid-derived suppressor cell-like cells are closely related to the clinical severity of multiple sclerosis.Acta neuropathologica · 2023Article
- Sex Differences in Inflammation and Muscle Wasting in Aging and Disease.International journal of molecular sciences · 2023Review
- Nano-Immunomodulation: A New Strategy for Skeletal Muscle Diseases and Aging?International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dystrophic muscle is characterized by chronic injury and a steady recruitment of inflammatory Ly6Chi monocytes. Recent studies have identified the spleen as the dominant reservoir of these cells during chronic inflammation. Here, we investigated the contribution of splenic Ly6Chi monocytes to dystrophic muscle pathology. Using the mdx mouse model of muscular dystrophy, we show that Ly6Chi monocytes accumulate in great numbers in the spleen over the course of the disease. The chemokine receptor CCR2 was upregulated on Ly6Chi monocytes in mdx spleen before disease onset, thereby enabling their recruitment to dystrophic muscle. Splenectomy performed before disease onset significantly reduced the number of Ly6Chi monocytes infiltrating dystrophic limb muscle. Moreover, in the absence of splenic Ly6Chi monocytes there was a significant reduction in dystrophic muscle inflammation and necrosis, along with improved regeneration during early disease. However, during late disease, a lack of splenic Ly6Chi monocytes adversely affected muscle fiber repair, due to a delay in the phenotypic shift of proinflammatory F4/80+Ly6ChiCD206lo to antiinflammatory F4/80+Ly6CloCD206+ macrophages. Overall, we show that the spleen is an indispensable source of Ly6Chi monocytes in muscular dystrophy and that splenic monocytes are critical players in both muscle fiber injury and repair.
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