Evidence map›Paper›PMID 31656622›Full record

ArticleJRSM cardiovascular disease

Autophagy in the heart is enhanced and independent of disease progression in mus musculus dystrophinopathy models.

H R Spaulding, C Ballmann, J C Quindry, M B Hudson, J T Selsby

Open access · hybridAbstract read
In one paragraph

Article in JRSM cardiovascular disease. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.2field-weighted citation impact, top 47% 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

4 citing papers in PubMed, 4 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

5 authors at 4 institutions in 1 country.

H R SpauldingDepartment of Animal Science, Iowa State University, Ames, USA.ORCID https://orcid.org/0000-0002-2931-2775
C BallmannDepartment of Kinesiology, Samford University, Birmingham, USA.
J C QuindryHealth and Human Performance, University of Montana, Missoula, USA.ORCID https://orcid.org/0000-0003-4655-0086
M B HudsonDepartment of Kinesiology and Applied Physiology, University of Delaware, Newark, USA.
J T SelsbyDepartment of Animal Science, Iowa State University, Ames, USA.ORCID https://orcid.org/0000-0003-3797-7539
Iowa State University · USSamford University · USUniversity of Delaware · USUniversity of Montana · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDuchenne muscular dystrophy is a muscle wasting disease caused by dystrophin gene mutations resulting in dysfunctional dystrophin protein. Autophagy, a proteolytic process, is impaired in dystrophic skeletal muscle though little is known about the effect of dystrophin deficiency on autophagy in cardiac muscle. We hypothesized that with disease progression autophagy would become increasingly dysfunctional based upon indirect autophagic markers.

methodsMarkers of autophagy were measured by western blot in 7-week-old and 17-month-old control (C57) and dystrophic (mdx) hearts.

resultsCounter to our hypothesis, markers of autophagy were similar between groups. Given these surprising results, two independent experiments were conducted using 14-month-old mdx mice or 10-month-old mdx/Utrn

conclusionTogether these data suggest that autophagy is not impaired in the dystrophic myocardium as it is in dystrophic skeletal muscle and that disease progression and related injury is independent of autophagic dysfunction.

Indexed as

Duchenne muscular dystrophyheartmdxutrophin

Identifiers

PMID31656622
PMCPMC6790947
OpenAlexW2978310708

What OpenQuestion holds

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LicenceCC BY-NC
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.