Evidence map›Paper›PMID 15831533›Full record

ArticleThe Journal of physiology2005

Impaired voluntary running capacity of creatine kinase-deficient mice.

Iman Momken, Patrick Lechêne, Nathalie Koulmann, Dominique Fortin, Philippe Mateo, Bich Thuy Doan, Jacqueline Hoerter, Xavier Bigard, Vladimir Veksler, Renée Ventura-Clapier

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

35 citing papers in PubMed, 91 citations in OpenAlex.

  1. Article
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  7. Energetic Interactions Between Subcellular Organelles in Striated Muscles.Frontiers in cell and developmental biology · 2020
    Review
  8. Article
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  10. Cardiac protein expression patterns are associated with distinct inborn exercise capacity in non-selectively bred rats.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2018
    Article
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  16. Review
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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

10 authors at 2 institutions in 2 countries.

Iman MomkenCellular and Molecular Cardiology, INSERM U-446, Pharmacy Faculty, Paris South University, Châtenay-Malabry, France.
Patrick Lechêne
Nathalie Koulmann
Dominique Fortin
Philippe Mateo
Bich Thuy Doan
Jacqueline Hoerter
Xavier Bigard
Vladimir Veksler
Renée Ventura-Clapier
Inserm · FRSouth University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The creatine kinase system (CK) is important for energy delivery in skeletal and cardiac muscles. The two main isoforms of this enzyme, cytosolic MM-CK and mitochondrial mi-CK, are expressed in a developmental and muscle-type specific manner. Mice deficient in one or both of these isoforms are viable and fertile but exhibit profound functional, metabolic and structural muscle remodelling that primarily affects fast skeletal muscles, which show an increased contribution of oxidative metabolism to contractile function. However, the consequences of these alterations in terms of physical capabilities have not yet been characterized. Consequently, we compared the voluntary exercise capacity of 9-month-old male wild-type (WT), M-CK knockout (M-CK(-/-)), and M-CK and mi-CK double knockout (CK(-/-)) mice, using cages equipped with running wheels. Exercise performance, calculated by total distance covered and by work done during the training period, was more than 10-fold lower in CK(-/-) mice than controls, with M-CK(-/-) mice exhibiting intermediate performance. Similarly, the mean distance run per activation was lower in M-CK(-/-) and even lower in CK(-/-) mice. However, the maximal running speed (V(max)) was lower only for CK(-/-) mice. This was accompanied by severe skeletal muscle mass decrease in CK(-/-) mice, with signs of histological damage that included enlarged interstitial areas, aggregations of mononuclear cells in the interstitium, heterogeneity of myofibre size and the presence of very small fibres. No overt sign of cardiac dysfunction was observed by magnetic resonance imaging during dobutamine stimulation. These results show that metabolic failure induced by CK deficiency profoundly affects the ability of mice to engage in chronic bouts of endurance running exercise and that this decrease in performance is also associated with muscle wasting.

Indexed as

AnimalsBody WeightCreatine KinaseCreatine Kinase, Mitochondrial FormCreatine Kinase, MM FormGene ExpressionIsoenzymesMiceMice, Inbred C57BLMice, KnockoutMuscle ContractionMuscle, SkeletalMuscular AtrophyMyocardial ContractionMyocardiumMyosin Heavy ChainsCreatine KinaseCreatine Kinase, Mitochondrial FormCreatine Kinase, MM FormIsoenzymesMyosin Heavy Chains

Identifiers

PMID15831533
PMCPMC1464549
OpenAlexW1583314060

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.