ArticleScientific reports2017
Levels of S100B protein drive the reparative process in acute muscle injury and muscular dystrophy.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 43 citations in OpenAlex.
- Soluble RAGE enhances muscle regeneration after cryoinjury in aged and diseased mice.PloS one · 2025Article
- Targeting the AGEs-RAGE axis: pathogenic mechanisms and therapeutic interventions in diabetic wound healing.Frontiers in medicine · 2025Review
- The MyoGravity project to study real microgravity effects on human muscle precursor cells and tissue.NPJ microgravity · 2024Article
- Respiratory neuropathology in spinocerebellar ataxia type 7.JCI insight · 2024Article
- Damage-mediated macrophage polarization in sterile inflammation.Frontiers in immunology · 2023Review
- Human Adipose-Derived Stromal Cells Delivered on Decellularized Muscle Improve Muscle Regeneration and Regulate RAGE and P38 MAPK.Bioengineering (Basel, Switzerland) · 2022Article
- Article
- Intracellular Protein S-Nitrosylation-A Cells Response to Extracellular S100B and RAGE Receptor.Biomolecules · 2022Article
- TLR4 is a regulator of trained immunity in a murine model of Duchenne muscular dystrophy.Nature communications · 2022Article
- Preliminary Study of S100B and Sema3A Expression Patterns in Regenerating Muscle Implicates P75-Expressing Terminal Schwann Cells and Muscle Satellite Cells in Neuromuscular Junction Restoration.Frontiers in cell and developmental biology · 2022Article
- Unilateral vagotomy alters astrocyte and microglial morphology in the nucleus tractus solitarii of the rat.American journal of physiology. Regulatory, integrative and comparative physiology · 2021Article
- Targeting RAGE to prevent SARS-CoV-2-mediated multiple organ failure: Hypotheses and perspectives.Life sciences · 2021Review
- Sarcopenia in Chronic Kidney Disease: Focus on Advanced Glycation End Products as Mediators and Markers of Oxidative Stress.Biomedicines · 2021Review
- Identification of Macrophage Polarization-Related Genes as Biomarkers of Chronic Obstructive Pulmonary Disease Based on Bioinformatics Analyses.BioMed research international · 2021Article
- Cancer-Associated Muscle Wasting-Candidate Mechanisms and Molecular Pathways.International journal of molecular sciences · 2020Review
- Response by Sreejit and Nagareddy to Letter Regarding Article, "Neutrophil-Derived S100A8/A9 Amplify Granulopoiesis After Myocardial Infarction".Circulation · 2020Article
- Targeting RAGE prevents muscle wasting and prolongs survival in cancer cachexia.Journal of cachexia, sarcopenia and muscle · 2020Article
- S100 proteins in obesity: liaisons dangereuses.Cellular and molecular life sciences : CMLS · 2020Review
- Expression of S100B Protein in Ischemia/Reperfusion-Induced Brain Injury After Cyclosporine Therapy: A Biochemical Serum Marker with Prognostic Value?Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- RAGE in the pathophysiology of skeletal muscle.Journal of cachexia, sarcopenia and muscle · 2018Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Regeneration of injured skeletal muscles relies on a tightly controlled chain of cellular and molecular events. We show that appropriate levels of S100B protein are required for timely muscle regeneration after acute injury. S100B released from damaged myofibers and infiltrating macrophages expands the myoblast population, attracts macrophages and promotes their polarization into M2 (pro-regenerative) phenotype, and modulates collagen deposition, by interacting with RAGE (receptor for advanced glycation end-products) or FGFR1 (fibroblast growth factor receptor 1) depending on the muscle repair phase and local conditions. However, persistence of high S100B levels compromises the regeneration process prolonging myoblast proliferation and macrophage infiltration, delaying M1/M2 macrophage transition, and promoting deposition of fibrotic tissue via RAGE engagement. Interestingly, S100B is released in high abundance from degenerating muscles of mdx mice, an animal model of Duchenne muscular dystrophy (DMD), and blocking S100B ameliorates histopathology. Thus, levels of S100B differentially affect skeletal muscle repair upon acute injury and in the context of muscular dystrophy, and S100B might be regarded as a potential molecular target in DMD.
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