Evidence map›Paper›PMID 20508850›Full record

ArticleJournal of biomedicine & biotechnology2010

Proteomic Profiling of the Dystrophin-Deficient MDX Heart Reveals Drastically Altered Levels of Key Metabolic and Contractile Proteins.

Caroline Lewis, Harald Jockusch, Kay Ohlendieck

Open access · hybridAbstract read
In one paragraph

Article in Journal of biomedicine & biotechnology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

16 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. Identification of Ubiquitination-Associated Proteins Using 2D-DIGE.Methods in molecular biology (Clifton, N.J.) · 2023
    Article
  4. Bioinformatic Analysis of the Subproteomic Profile of Cardiomyopathic Tissue.Methods in molecular biology (Clifton, N.J.) · 2023
    Article
  5. Review
  6. Review
  7. Therapeutic potential of heat shock protein induction for muscular dystrophy and other muscle wasting conditions.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2018
    Review
  8. Transient receptor potential channel 6 regulates abnormal cardiac S-nitrosylation in Duchenne muscular dystrophy.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  9. Article
  10. Blockade of ActRIIB signaling triggers muscle fatigability and metabolic myopathy.Molecular therapy : the journal of the American Society of Gene Therapy · 2014
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
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 2 countries.

Caroline LewisDepartment of Biology, National University of Ireland, Maynooth, Kildare, Ireland.
Harald Jockusch
Kay Ohlendieck
National University of Ireland, Maynooth · IEBielefeld University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although Duchenne muscular dystrophy is primarily classified as a neuromuscular disease, cardiac complications play an important role in the course of this X-linked inherited disorder. The pathobiochemical steps causing a progressive decline in the dystrophic heart are not well understood. We therefore carried out a fluorescence difference in-gel electrophoretic analysis of 9-month-old dystrophin-deficient versus age-matched normal heart, using the established MDX mouse model of muscular dystrophy-related cardiomyopathy. Out of 2,509 detectable protein spots, 79 2D-spots showed a drastic differential expression pattern, with the concentration of 3 proteins being increased, including nucleoside diphosphate kinase and lamin-A/C, and of 26 protein species being decreased, including ATP synthase, fatty acid binding-protein, isocitrate dehydrogenase, NADH dehydrogenase, porin, peroxiredoxin, adenylate kinase, tropomyosin, actin, and myosin light chains. Hence, the lack of cardiac dystrophin appears to trigger a generally perturbed protein expression pattern in the MDX heart, affecting especially energy metabolism and contractile proteins.

Identifiers

PMID20508850
PMCPMC2874991
OpenAlexW2058628988

What OpenQuestion holds

Textmetadata
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.