ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2011
Acute skeletal muscle injury: CCL2 expression by both monocytes and injured muscle is required for repair.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 159 papers.
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The trial behind it
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Who cites it
159 citing papers in PubMed, 252 citations in OpenAlex.
- Improved recovery from skeletal muscle damage is largely unexplained by myofibrillar protein synthesis or inflammatory and regenerative gene expression pathways.American journal of physiology. Endocrinology and metabolism · 2021Trial
- Human skeletal muscle macrophages increase following cycle training and are associated with adaptations that may facilitate growth.Scientific reports · 2019Trial
- Effect of cryotherapy on muscle recovery and inflammation following a bout of damaging exercise.European journal of applied physiology · 2013Trial
- Review
- Glucocorticoid Receptor Signaling in Myeloid Cells Orchestrates Inflammation Resolution and Muscle Repair.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- FAP-derived CCL2 is required for adequate monocyte/macrophage infiltration to support acute skeletal muscle injury repair.iScience · 2026Article
- Mesenchymal Stromal Cell-Mediated Intercellular Communication: Mapping the Interactome for Skeletal Muscle Homeostasis and Regeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Senescence dynamics define therapeutic windows for Duchenne muscular dystrophy in DBA/2-mdx mice.Skeletal muscle · 2026Article
- SMCHD1 loss re-wires MYOD1 enhancer nexuses and chromatin accessibility landscapes in muscle cells.bioRxiv : the preprint server for biology · 2026Article
- Macrophage Infiltration, Activation, and Therapeutic Implication in Skeletal Muscle Injury and Repair.International journal of molecular sciences · 2026Review
- Gait, skin and coat, and plasma cytokine changes in response to exercise and trace mineral source.Journal of animal science · 2026Article
- Targeting efferocytosis for tissue regeneration: From microenvironment reprogramming to clinical translation.Theranostics · 2026Review
- Macrophage plasticity and metabolic control in muscle repair and disease.Frontiers in immunology · 2026Review
- Doxorubicin Impairs Skeletal Muscle Regeneration by Dysregulating the Early Inflammatory Response.FASEB bioAdvances · 2025Article
- CXCL14 Promotes Skeletal Muscle Mass Growth and Attenuates Lipopolysaccharide- and Dexamethasone-Induced Muscle Atrophy in Cultured Myotubes and Mouse Models.Journal of cachexia, sarcopenia and muscle · 2025Article
- Satellite cells choreograph an immune cell-fibrogenic cell circuit during mechanical loading in geriatric skeletal muscle.PNAS nexus · 2025Article
- Investigation of the Effects of Silicon Dioxide Nanoparticles and Environmental Contaminants on Immunocytotoxic and Antioxidant Defense Systems in Model Organism Galleria mellonella L.Biological trace element research · 2025Article
- Heterogeneous Macrophage Activation in Acute Skeletal Muscle Sterile Injury andInternational journal of molecular sciences · 2025Article
- Repeated bouts of load carriage alter indirect markers of exercise-induced muscle damage, liver enzymes, and oxygen-carrying capacity in male soldiers.Physiological reports · 2025Article
- Macrophages: Subtypes, Distribution, Polarization, Immunomodulatory Functions, and Therapeutics.MedComm · 2025Review
99 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
CC chemokine ligand 2 (CCL2), a ligand of CC chemokine receptor 2 (CCR2), is essential to mount an adequate inflammatory response to repair acute skeletal muscle injury. We studied the mechanisms by which CCL2 regulates muscle inflammation and regeneration. Mobilization of monocytes/macrophages (MOs/MPs) but not lymphocytes or neutrophils was impaired from bone marrow to blood and from blood to injured muscles in Ccl2(-/-) mice. This was accompanied by poor phagocytosis, reduced up-regulation of insulin-like growth factor-1 (IGF-1), and impaired muscle regeneration. Bone marrow transfer from wild-type mice to irradiated Ccr2(-/-) but not Ccl2(-/-) mice restored muscle inflammation. Intravenously injected CCL2-deficient bone marrow monocytes could not enter wild-type injured muscles as well as wild-type bone marrow monocytes. Intravenously injected wild-type bone marrow monocytes could not enter CCL2-deficient injured muscles as well as wild-type injured muscles. CCL2 stimulated IGF-1 expression by wild-type but not CCR2-deficient intramuscular macrophages. A single intramuscular injection of IGF-1, but not PBS, markedly improved muscle regeneration in Ccl2(-/-) mice. We conclude that CCL2 is a major ligand of CCR2 to recruit MOs/MPs into injured muscles to conduct phagocytosis and produce IGF-1 for injury repair. CCL2 needs to be expressed by bone marrow cells, circulating monocytes, and injured muscle tissue cells to recruit MOs/MPs into injured muscles. CCL2/CCR2 signaling also up-regulates IGF-1 expression by intramuscular macrophages to promote acute skeletal muscle injury repair.
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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.