Evidence map›Paper›PMID 16767467›Full record

ReviewPflugers Archiv : European journal of physiology2006

Heart failure: a model of cardiac and skeletal muscle energetic failure.

B Mettauer, J Zoll, A Garnier, R Ventura-Clapier

Abstract readReview
PubMed Publisher
In one paragraph

Review in Pflugers Archiv : European journal of physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

23 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
  2. Molecular mechanisms underlying sarcopenia in heart failure.The journal of cardiovascular aging · 2024
    Article
  3. Iron Deficiency and Deranged Myocardial Energetics in Heart Failure.International journal of environmental research and public health · 2022
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Skeletal muscle alterations in HFrEF vs. HFpEF.Current heart failure reports · 2017
    Review
  10. Maintaining PGC-1α expression following pressure overload-induced cardiac hypertrophy preserves angiogenesis but not contractile or mitochondrial function.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014
    Article
  11. Review
  12. Article
  13. Skeletal muscle protein metabolism in human heart failure.Current opinion in clinical nutrition and metabolic care · 2013
    Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Skeletal muscle dysfunction in muscle-specific LKB1 knockout mice.Journal of applied physiology (Bethesda, Md. : 1985) · 2010
    Article
  20. 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

4 authors at 2 institutions in 1 country.

B MettauerDépartement de Physiologie, CHRU, EA3072, F-67091 Strasbourg, France. bertrand.mettauer@ch-colmar.rss.fr
J Zoll
A Garnier
R Ventura-Clapier
Hôpitaux Universitaires de Strasbourg · FRUniversité Paris-Sud · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic heart failure (CHF), the new epidemic in cardiology, is characterized by energetic failure of both cardiac and skeletal muscles. The failing heart wastes energy due to anatomical changes that include cavity enlargement, altered geometry, tachycardia, mitral insufficiency and abnormal loading, while skeletal muscle undergoes atrophy. Cardiac and skeletal muscles also have altered high-energy phosphate production and handling in CHF. Nevertheless, there are differences in the phenotype of myocardial and skeletal muscle myopathy in CHF: cardiomyocytes have a lower mitochondrial oxidative capacity, abnormal substrate utilisation and intracellular signalling but a maintained oxidative profile; in skeletal muscle, by contrast, mitochondrial failure is less clear, and there is altered microvascular reactivity, fibre type shifts and abnormalities in the enzymatic systems involved in energy distribution. Underlying these phenotypic abnormalities are changes in gene regulation in both cardiac and skeletal muscle cells. Here, we review the latest advances in cardiac and skeletal muscle energetic research and argue that energetic failure could be taken as a unifying mechanism leading to contractile failure, ultimately resulting in skeletal muscle energetic failure, exertional fatigue and death.

Indexed as

AnimalsChronic DiseaseEnergy MetabolismHeartHeart FailureHumansMuscle CellsMuscle, Skeletal

Identifiers

PMID16767467
OpenAlexW2030702573

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.