ArticleEMBO molecular medicine2014
Inflammatory monocytes promote progression of Duchenne muscular dystrophy and can be therapeutically targeted via CCR2.
Article in EMBO molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
90 citing papers in PubMed, 1 synthesis or guideline pooled it, 167 citations in OpenAlex.
- Pooled it
- Long-term imoxin treatment does not attenuate disease severity in dystrophic diaphragm of male mice.Physiological reports · 2026Article
- FAP-derived CCL2 is required for adequate monocyte/macrophage infiltration to support acute skeletal muscle injury repair.iScience · 2026Article
- RUNX2 Activation in Fibro/Adipogenic Progenitors Promotes Muscle Fibrosis in Muscular Dystrophy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 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
- Unraveling the pleiotropic effects of CCR2-dependent signal transduction in fibrosis development.Theranostics · 2026Review
- Heterogeneous Macrophage Activation in Acute Skeletal Muscle Sterile Injury andInternational journal of molecular sciences · 2025Article
- Article
- Macrophage Subpopulation Promotes Skeletal Muscle Regeneration Through HGF/MET Signaling-Mediated Skeletal Muscle Stem Cell Proliferation.Aging cell · 2025Article
- Expansion and pathogenic activation of skeletal muscle-resident macrophages inProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Inhibiting EZH2 complements steroid effects in Duchenne muscular dystrophy.Science advances · 2025Article
- Circulatory CCL2 distinguishes Duchenne muscular dystrophy dogs.Disease models & mechanisms · 2025Article
- Macrophages in the Context of Muscle Regeneration and Duchenne Muscular Dystrophy.International journal of molecular sciences · 2024Review
- Muscle cell-derived Ccl8 is a negative regulator of skeletal muscle regeneration.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Exploring lipin1 as a promising therapeutic target for the treatment of Duchenne muscular dystrophy.Journal of translational medicine · 2024Article
- Recent Advances in Pre-Clinical Development of Adiponectin Receptor Agonist Therapies for Duchenne Muscular Dystrophy.Biomedicines · 2024Review
- Identification of hub genes and therapeutic siRNAs to develop novel adjunctive therapy for Duchenne muscular dystrophy.BMC musculoskeletal disorders · 2024Article
- Dynamic equilibrium of skeletal muscle macrophage ontogeny in the diaphragm during homeostasis, injury, and recovery.Scientific reports · 2024Article
- Regenerative inflammation: When immune cells help to re-build tissues.The FEBS journal · 2024Review
30 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
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Myofiber necrosis and fibrosis are hallmarks of Duchenne muscular dystrophy (DMD), leading to lethal weakness of the diaphragm. Macrophages (MPs) are required for successful muscle regeneration, but the role of inflammatory monocyte (MO)-derived MPs in either promoting or mitigating DMD is unclear. We show that DMD (mdx) mouse diaphragms exhibit greatly increased expression of CCR2 and its chemokine ligands, along with inflammatory (Ly6C(high)) MO recruitment and accumulation of CD11b(high) MO-derived MPs. Loss-of-function of CCR2 preferentially reduced this CD11b(high) MP population by impeding the release of Ly6C(high) MOs from the bone marrow but not the splenic reservoir. CCR2 deficiency also helped restore the MP polarization balance by preventing excessive skewing of MPs toward a proinflammatory phenotype. These effects were linked to amelioration of histopathological features and increased muscle strength in the diaphragm. Chronic inhibition of CCR2 signaling by mutated CCL2 secreted from implanted mesenchymal stem cells resulted in similar improvements. These data uncover a previously unrecognized role of inflammatory MOs in DMD pathogenesis and indicate that CCR2 inhibition could offer a novel strategy for DMD management.
Indexed as
Identifiers
What OpenQuestion holds
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.