Cited by 299Muscle Physiology and DisordersNeurogenetic and Muscular Disorders ResearchInflammatory Myopathies and Dermatomyositis

The DOI matches its Crossref record; 67 of the 67 references it cites were found in a registry or an index.

Interleukin-10 reduces the pathology of mdx muscular dystrophy by deactivating M1 macrophages and modulating macrophage phenotype

Open access
Villalta, S. A., Rinaldi, C., Deng, B., Liu, G., Fedor, B., Tidball, J. G.·2011·Human Molecular Genetics

Abstract

M1 macrophages play a major role in worsening muscle injury in the mdx mouse model of Duchenne muscular dystrophy. However, mdx muscle also contains M2c macrophages that can promote tissue repair, indicating that factors regulating the balance between M1 and M2c phenotypes could influence the severity of the disease. Because interleukin-10 (IL-10) modulates macrophage activation in vitro and its expression is elevated in mdx muscles, we tested whether IL-10 influenced the macrophage phenotype in mdx muscle and whether changes in IL-10 expression affected the pathology of muscular dystrophy. Ablation of IL-10 expression in mdx mice increased muscle damage in vivo and reduced mouse strength. Treating mdx muscle macrophages with IL-10 reduced activation of the M1 phenotype, assessed by iNOS expression, and macrophages from IL-10 null mutant mice were more cytolytic than macrophages isolated from wild-type mice. Our data also showed that muscle cells in mdx muscle expressed the IL-10 receptor, suggesting that IL-10 could have direct effects on muscle cells. We assayed whether ablation of IL-10 in mdx mice affected satellite cell numbers, using Pax7 expression as an index, but found no effect. However, IL-10 mutation significantly increased myogenin expression in vivo during the acute and the regenerative phase of mdx pathology. Together, the results show that IL-10 plays a significant regulatory role in muscular dystrophy that may be caused by reducing M1 macrophage activation and cytotoxicity, increasing M2c macrophage activation and modulating muscle differentiation.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1093/hmg/ddq523

Cites

67 of 67 references verified0 citation errors · 0 not checkable

Statistics

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Cited by

Sorted by citations

See all 299

Metadata

Authors
Villalta, S. A., Rinaldi, C., Deng, B., Liu, G., Fedor, B., & Tidball, J. G.
Affiliations
University of California, Los Angeles (US)
Corresponding author
Tidball, J. G.
Venue
Human Molecular Genetics
Published
2010-11-30
Volume
20
Issue
4
Pages
790-805
ISSN
  • 0964-6906 (ISSN-L)
  • 1460-2083
OpenAlex
W2149152441
Cited by
299
References
67
Citations by year
2026: 10 · 2025: 19 · 2024: 11 · 2023: 13 · 2022: 18 · 2021: 20 · 2020: 14 · 2019: 26 · 2018: 25 · 2017: 25 · 2016: 16 · 2015: 24 · 2014: 23 · 2013: 21 · 2012: 21
FWCI
7.17
Type
journal article
Language
en
Open access
Locations
  • Human Molecular Genetics (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Muscular Dystrophy Association (157881)
  • National Institutes of Health (5r01ar040343-12, AR40343)
  • National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01 AR47721, R01 AR 40343, R01AR047721, F31AR054724)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
  • Health Sciences › Medicine › Genetics (clinical) › Neurogenetic and Muscular Disorders Research
  • Health Sciences › Medicine › Rheumatology › Inflammatory Myopathies and Dermatomyositis
Keywords
IL-10, Duchenne muscular dystrophy, mdx mice, M1 macrophages, M2c macrophages, macrophage polarization, muscle damage, inducible nitric oxide synthase, macrophage cytotoxicity, IL-10 receptor, satellite cells, Pax7, myogenin, muscle regeneration, myogenesis
MeSH terms
Animals, Cell Differentiation, Cell Line, Macrophage Activation, Macrophages, Mice, Inbred C57BL, Phagocytosis, Phenotype, Regeneration, Interleukin-10, Mice, Inbred mdx, Muscle, Skeletal, Muscular Dystrophy, Duchenne, Mice, Receptors, Interleukin-10

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review