Evidence map›Paper›PMID 27634466›Full record

ArticleScientific reports2016

Progressive muscle proteome changes in a clinically relevant pig model of Duchenne muscular dystrophy.

Thomas Fröhlich, Elisabeth Kemter, Florian Flenkenthaler, Nikolai Klymiuk, Kathrin A Otte, Andreas Blutke, Sabine Krause, Maggie C Walter, Rüdiger Wanke, Eckhard Wolf and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

47 citing papers in PubMed, 78 citations in OpenAlex.

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  12. Systemic deletion ofProceedings of the National Academy of Sciences of the United States of America · 2023
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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 1 institution in 1 country.

Thomas FröhlichLaboratory for Functional Genome Analysis (LAFUGA), Gene Center, LMU Munich, Feodor-Lynen-Str. 25, D-81377 Munich, Germany.
Elisabeth KemterChair for Molecular Animal Breeding and Biotechnology, Gene Center and Department of Veterinary Sciences, LMU Munich, Feodor-Lynen-Str. 25, D-81377 Munich, Germany.
Florian FlenkenthalerLaboratory for Functional Genome Analysis (LAFUGA), Gene Center, LMU Munich, Feodor-Lynen-Str. 25, D-81377 Munich, Germany.
Nikolai KlymiukChair for Molecular Animal Breeding and Biotechnology, Gene Center and Department of Veterinary Sciences, LMU Munich, Feodor-Lynen-Str. 25, D-81377 Munich, Germany.
Kathrin A OtteLaboratory for Functional Genome Analysis (LAFUGA), Gene Center, LMU Munich, Feodor-Lynen-Str. 25, D-81377 Munich, Germany.
Andreas BlutkeInstitute of Veterinary Pathology, Centre for Clinical Veterinary Medicine, LMU Munich, Veterinärstr. 13, D-80539 Munich, Germany.
Sabine KrauseFriedrich-Baur-Institute, Department of Neurology, LMU Munich, Ziemssenstr. 1, D-80336 Munich, Germany.
Maggie C WalterFriedrich-Baur-Institute, Department of Neurology, LMU Munich, Ziemssenstr. 1, D-80336 Munich, Germany.
Rüdiger WankeInstitute of Veterinary Pathology, Centre for Clinical Veterinary Medicine, LMU Munich, Veterinärstr. 13, D-80539 Munich, Germany.
Eckhard WolfLaboratory for Functional Genome Analysis (LAFUGA), Gene Center, LMU Munich, Feodor-Lynen-Str. 25, D-81377 Munich, Germany.
Georg J ArnoldLaboratory for Functional Genome Analysis (LAFUGA), Gene Center, LMU Munich, Feodor-Lynen-Str. 25, D-81377 Munich, Germany.
Ludwig-Maximilians-Universität München · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Duchenne muscular dystrophy (DMD) is caused by genetic deficiency of dystrophin and characterized by massive structural and functional changes of skeletal muscle tissue, leading to terminal muscle failure. We recently generated a novel genetically engineered pig model reflecting pathological hallmarks of human DMD better than the widely used mdx mouse. To get insight into the hierarchy of molecular derangements during DMD progression, we performed a proteome analysis of biceps femoris muscle samples from 2-day-old and 3-month-old DMD and wild-type (WT) pigs. The extent of proteome changes in DMD vs. WT muscle increased markedly with age, reflecting progression of the pathological changes. In 3-month-old DMD muscle, proteins related to muscle repair such as vimentin, nestin, desmin and tenascin C were found to be increased, whereas a large number of respiratory chain proteins were decreased in abundance in DMD muscle, indicating serious disturbances in aerobic energy production and a reduction of functional muscle tissue. The combination of proteome data for fiber type specific myosin heavy chain proteins and immunohistochemistry showed preferential degeneration of fast-twitch fiber types in DMD muscle. The stage-specific proteome changes detected in this large animal model of clinically severe muscular dystrophy provide novel molecular readouts for future treatment trials.

Indexed as

AgingAnimalsDisease Models, AnimalDystrophinImmunohistochemistryMitochondrial ProteinsMuscle Fibers, Fast-TwitchMuscle Fibers, Slow-TwitchMuscle ProteinsMuscle, SkeletalMuscular Dystrophy, AnimalMyosin Heavy ChainsProteomeSus scrofaDystrophinMitochondrial ProteinsMuscle ProteinsMyosin Heavy ChainsProteome

Identifiers

PMID27634466
PMCPMC5025886
OpenAlexW2519710080

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.