Evidence map›Paper›PMID 28281577›Full record

ArticleScientific reports2017

Potent pro-inflammatory and pro-fibrotic molecules, osteopontin and galectin-3, are not major disease modulators of laminin α2 chain-deficient muscular dystrophy.

Kinga I Gawlik, Johan Holmberg, Martina Svensson, Mikaela Einerborg, Bernardo M S Oliveira, Tomas Deierborg, Madeleine Durbeej

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

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  12. Fibrogenesis inFrontiers in molecular neuroscience · 2020
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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

7 authors at 1 institution in 1 country.

Kinga I GawlikDepartment of Experimental Medical Science, Muscle Biology Unit, Lund University, Sweden.
Johan HolmbergDepartment of Experimental Medical Science, Muscle Biology Unit, Lund University, Sweden.
Martina SvenssonDepartment of Experimental Medical Science, Experimental Neuroinflammation Laboratory, Lund University, Sweden.
Mikaela EinerborgDepartment of Experimental Medical Science, Muscle Biology Unit, Lund University, Sweden.
Bernardo M S OliveiraDepartment of Experimental Medical Science, Muscle Biology Unit, Lund University, Sweden.
Tomas DeierborgDepartment of Experimental Medical Science, Experimental Neuroinflammation Laboratory, Lund University, Sweden.
Madeleine DurbeejDepartment of Experimental Medical Science, Muscle Biology Unit, Lund University, Sweden.
Lund University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A large number of human diseases are caused by chronic tissue injury with fibrosis potentially leading to organ failure. There is a need for more effective anti-fibrotic therapies. Congenital muscular dystrophy type 1A (MDC1A) is a devastating form of muscular dystrophy caused by laminin α2 chain-deficiency. It is characterized with early inflammation and build-up of fibrotic lesions, both in patients and MDC1A mouse models (e.g. dy

Indexed as

AnimalsFemaleFibrosisGalectin 3InflammationInflammation MediatorsLamininMaleMice, KnockoutMuscle, SkeletalMuscular DystrophiesMuscular Dystrophy, AnimalOsteopontinPhenotypeGalectin 3Inflammation MediatorsLamininlaminin alpha 2Lgals3 protein, mouseOsteopontinSpp1 protein, mouse

Identifiers

PMID28281577
PMCPMC5345027
OpenAlexW2594550096

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.