Evidence map›Paper›PMID 29259687›Full record

ReviewInflammation and regeneration2016

Inflammatory predisposition predicts disease phenotypes in muscular dystrophy.

Yuko Nitahara-Kasahara, Shin'ichi Takeda, Takashi Okada

Open access · goldAbstract readReview
In one paragraph

Review in Inflammation and regeneration, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

18 citing papers in PubMed, 30 citations in OpenAlex.

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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

3 authors at 2 institutions in 1 country.

Yuko Nitahara-KasaharaDepartment of Biochemistry and Molecular Biology, Nippon Medical School, Bunkyo-ku Tokyo, Japan.
Shin'ichi TakedaDepartment of Molecular Therapy, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira Tokyo, Japan.
Takashi OkadaDepartment of Biochemistry and Molecular Biology, Nippon Medical School, Bunkyo-ku Tokyo, Japan.
Nippon Medical School · JPNational Center of Neurology and Psychiatry · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Duchenne muscular dystrophy is an incurable genetic disease that presents with skeletal muscle weakness and chronic inflammation and is associated with early mortality. Indeed, immune cell infiltration into the skeletal muscle is a notable feature of the disease pathophysiology and is strongly associated with disease severity. Interleukin (IL)-10 regulates inflammatory immune responses by reducing both M1 macrophage activation and the production of pro-inflammatory cytokines, thereby promoting the activation of the M2 macrophage phenotype. We previously reported that genetic ablation of IL-10 in dystrophic mice resulted in more severe phenotypes, in regard to heart and respiratory function, as evidenced by increased macrophage infiltration, high levels of inflammatory factors in the muscle, and progressive cardiorespiratory dysfunction. These data therefore indicate that IL-10 comprises an essential immune-modulator within dystrophic muscles. In this review, we highlight the pivotal role of the immune system in the pathogenesis of muscular dystrophy and discuss how an increased understanding of the pathogenesis of this disease may lead to novel therapeutic strategies.

Indexed as

Animal modelAnti-inflammationIL-10Muscular dystrophy

Identifiers

PMID29259687
PMCPMC5725653
OpenAlexW2518934106

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.