Evidence map›Paper›PMID 26137572›Full record

ArticleEBioMedicine2015

Functional and Morphological Improvement of Dystrophic Muscle by Interleukin 6 Receptor Blockade.

Laura Pelosi, Maria Grazia Berardinelli, Loredana De Pasquale, Carmine Nicoletti, Adele D'Amico, Francesco Carvello, Gian Marco Moneta, Angela Catizone, Enrico Bertini, Fabrizio De Benedetti and 1 more

Open access · goldAbstract read
In one paragraph

Article in EBioMedicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 5% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

56 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.

  1. Pooled it
  2. Review
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  5. Lymphatic dysfunction is linked to disease pathogenesis in Duchenne muscular dystrophy animal models.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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  9. Delivery of A Chemically Modified Noncoding RNA Domain Improves Dystrophic Myotube Function.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
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  11. [Benefits of ω-3 fatty acids in Duchenne muscular dystrophy].Revista medica del Instituto Mexicano del Seguro Social · 2025
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 1 country.

Laura PelosiInstitute Pasteur-Cenci Bolognetti, DAHFMO-Unit of Histology and Medical Embryology, IIM, Sapienza University of Rome, 00161, Italy.
Maria Grazia BerardinelliInstitute Pasteur-Cenci Bolognetti, DAHFMO-Unit of Histology and Medical Embryology, IIM, Sapienza University of Rome, 00161, Italy.
Loredana De PasqualeDivision of Rheumatology, Bambino Gesù Children's Hospital, Rome 00100, Italy.
Carmine NicolettiInstitute Pasteur-Cenci Bolognetti, DAHFMO-Unit of Histology and Medical Embryology, IIM, Sapienza University of Rome, 00161, Italy.
Adele D'AmicoDepartment of Neuroscience, Unit of Neuromuscular and Neurodegenerative Disease, Bambino Gesù Children's Hospital, Rome 00100, Italy.
Francesco CarvelloDivision of Rheumatology, Bambino Gesù Children's Hospital, Rome 00100, Italy.
Gian Marco MonetaDivision of Rheumatology, Bambino Gesù Children's Hospital, Rome 00100, Italy.
Angela CatizoneInstitute Pasteur-Cenci Bolognetti, DAHFMO-Unit of Histology and Medical Embryology, IIM, Sapienza University of Rome, 00161, Italy.
Enrico BertiniDepartment of Neuroscience, Unit of Neuromuscular and Neurodegenerative Disease, Bambino Gesù Children's Hospital, Rome 00100, Italy.
Fabrizio De BenedettiDivision of Rheumatology, Bambino Gesù Children's Hospital, Rome 00100, Italy.
Antonio MusaròInstitute Pasteur-Cenci Bolognetti, DAHFMO-Unit of Histology and Medical Embryology, IIM, Sapienza University of Rome, 00161, Italy ; Center for Life Nano Science@Sapienza, Istituto Italiano di Tecnologia, Rome 00161, Italy.
Bambino Gesù Children's Hospital · ITIstituto Pasteur · ITItalian Institute of Technology · IT

Funding

Telethon GGP13013
6 · The paper itself

Abstract

The anti-inflammatory agents glucocorticoids (GC) are the only available treatment for Duchenne muscular dystrophy (DMD). However, long-term GC treatment causes muscle atrophy and wasting. Thus, targeting specific mediator of inflammatory response may be more specific, more efficacious, and with fewer side effects. The pro-inflammatory cytokine interleukin (IL) 6 is overproduced in patients with DMD and in the muscle of mdx, the animal model for human DMD. We tested the ability of inhibition of IL6 activity, using an interleukin-6 receptor (Il6r) neutralizing antibody, to ameliorate the dystrophic phenotype. Blockade of endogenous Il6r conferred on dystrophic muscle resistance to degeneration and alleviated both morphological and functional consequences of the primary genetic defect. Pharmacological inhibition of IL6 activity leaded to changes in the dystrophic muscle environment, favoring anti-inflammatory responses and improvement in muscle repair. This resulted in a functional homeostatic maintenance of dystrophic muscle. These data provide an alternative pharmacological strategy for treatment of DMD and circumvent the major problems associated with conventional therapy.

Indexed as

AnimalsDisease Models, AnimalHomeostasisInflammationInterleukin-6MaleMice, Inbred C57BLMice, Inbred mdxMusclesMuscular Dystrophy, AnimalMuscular Dystrophy, DuchenneNecrosisPhenotypeReceptors, Interleukin-6Interleukin-6Receptors, Interleukin-6IL6InflammationMuscular dystrophyNecrosisTherapy

Identifiers

PMID26137572
PMCPMC4485902
OpenAlexW2148366639

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.