Evidence map›Paper›PMID 28845212›Full record

ArticleOxidative medicine and cellular longevity2017

Increased Circulating Levels of Interleukin-6 Induce Perturbation in Redox-Regulated Signaling Cascades in Muscle of Dystrophic Mice.

Laura Pelosi, Laura Forcina, Carmine Nicoletti, Bianca Maria Scicchitano, Antonio Musarò

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

20 citing papers in PubMed, 30 citations in OpenAlex.

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  11. A research update: Significance of cytokine storm and diaphragm in COVID-19.Current research in pharmacology and drug discovery · 2021
    Article
  12. Nutrition and microRNAs: Novel Insights to Fight Sarcopenia.Antioxidants (Basel, Switzerland) · 2020
    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

5 authors at 3 institutions in 2 countries.

Laura PelosiDAHFMO-Unit of Histology and Medical Embryology, Sapienza University of Rome, Laboratory affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, Rome, Italy.ORCID 0000-0003-3964-8157
Laura ForcinaDAHFMO-Unit of Histology and Medical Embryology, Sapienza University of Rome, Laboratory affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, Rome, Italy.ORCID 0000-0003-3446-7672
Carmine NicolettiDAHFMO-Unit of Histology and Medical Embryology, Sapienza University of Rome, Laboratory affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, Rome, Italy.ORCID 0000-0001-5896-2040
Bianca Maria ScicchitanoInstitute of Histology and Embryology, School of Medicine, Catholic University of the Sacred Heart, Rome, Italy.
Antonio MusaròDAHFMO-Unit of Histology and Medical Embryology, Sapienza University of Rome, Laboratory affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, Rome, Italy.ORCID 0000-0002-2944-9739
Istituto Pasteur · ITItalian Institute of Technology · ITUniversità Cattolica del Sacro Cuore · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Duchenne muscular dystrophy (DMD) is an X-linked genetic disease in which dystrophin gene is mutated, resulting in dysfunctional or absent dystrophin protein. The pathology of dystrophic muscle includes degeneration, necrosis with inflammatory cell invasion, regeneration, and fibrous and fatty changes. Nevertheless, the mechanisms by which the absence of dystrophin leads to muscle degeneration remain to be fully elucidated. An imbalance between oxidant and antioxidant systems has been proposed as a secondary effect of DMD. However, the significance and precise extent of the perturbation in redox signaling cascades is poorly understood. We report that mdx dystrophic mice are able to activate a compensatory antioxidant response at the presymptomatic stage of the disease. In contrast, increased circulating levels of IL-6 perturb the redox signaling cascade, even prior to the necrotic stage, leading to severe features and progressive nature of muscular dystrophy.

Indexed as

Signal TransductionAnimalsDiaphragmDisease Models, AnimalDisease ProgressionGene Expression RegulationInterleukin-6Mice, Inbred C57BLMice, Inbred mdxMuscle, SkeletalMuscular Dystrophy, AnimalNecrosisNF-E2-Related Factor 2Oxidation-ReductionReactive Oxygen SpeciesTime FactorsInterleukin-6Nfe2l2 protein, mouseNF-E2-Related Factor 2Reactive Oxygen Species

Identifiers

PMID28845212
PMCPMC5563418
OpenAlexW2744282267

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.