Evidence map›Paper›PMID 15792353›Full record

ArticleMolecular and cellular biochemistry2005

Compartmentation of energy metabolism in atrial myocardium of patients undergoing cardiac surgery.

Evelin Seppet, Margus Eimre, Nadezhda Peet, Kalju Paju, Ehte Orlova, Mati Ress, Sirje Kõvask, Andres Piirsoo, Valdur A Saks, Frank N Gellerich and 2 more

Abstract read
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In one paragraph

Article in Molecular and cellular biochemistry, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.0field-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

19 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Impaired oxidative phosphorylation in overtrained rat myocardium.Experimental and clinical cardiology · 2010
    Article
  13. Article
  14. Impact of dietary fatty acids on cardiac arrhythmogenesis.Circulation. Arrhythmia and electrophysiology · 2009
    Review
  15. Mitochondria in the human heart.Journal of bioenergetics and biomembranes · 2009
    Review
  16. Article
  17. Article
  18. Article
  19. Intracellular energetic units in healthy and diseased hearts.Experimental and clinical cardiology · 2005
    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

12 authors at 2 institutions in 2 countries.

Evelin SeppetDepartment of Pathophysiology, Human Genetics and Biology and Cardiovascular and Thoracic Surgery, Centre of Molecular and Clinical Medicine, Faculty of Medicine, University of Tartu, Tartu, Estonia.
Margus Eimre
Nadezhda Peet
Kalju Paju
Ehte Orlova
Mati Ress
Sirje Kõvask
Andres Piirsoo
Valdur A Saks
Frank N Gellerich
Stephan Zierz
Enn K Seppet
University of Tartu · EEMartin Luther University Halle-Wittenberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The parameters of oxidative phosphorylation and its interaction with creatine kinase (CK)- and adenylate kinase (AK)-phosphotransfer networks in situ were studied in skinned atrial fibers from 59 patients undergoing coronary artery bypass surgery, valve replacement/correction and atrial septal defect correction. In atria, the mitochondrial CK and AK are effectively coupled to oxidative phosphorylation, the MM-CK is coupled to ATPases and there exists a direct transfer of adenine nucleotides between mitochondria and ATPases. Elimination of cytoplasmic ADP with exogenous pyruvate kinase was not associated with a blockade of the stimulatory effects of creatine and AMP on respiration, neither could it abolish the coupling of MM-CK to ATPases and direct transfer of adenine nucleotides. Thus, atrial energy metabolism is compartmentalized so that mitochondria form functional complexes with adjacent ATPases. These complexes isolate a part of cellular adenine nucleotides from their cytoplasmic pool for participating in energy transfer via CK- and AK-networks, and/or direct exchange. Compared to atria in sinus rhythm, the fibrillating atria were larger and exhibited increased succinate-dependent respiration relative to glutamate-dependent respiration and augmented proton leak. Thus, alterations in mitochondrial oxidative phosphorylation may contribute to pathogenesis of atrial fibrillation.

Indexed as

Energy MetabolismAdenine NucleotidesAdenosine DiphosphateAdenosine MonophosphateAdenosine TriphosphatasesAdenosine TriphosphateAdenylate KinaseAdultCreatine KinaseCytoplasmDose-Response Relationship, DrugFemaleGlutamic AcidHeart AtriaHumansKineticsAdenine NucleotidesAdenosine DiphosphateAdenosine MonophosphateAdenosine TriphosphatasesAdenosine TriphosphateAdenylate KinaseCreatine KinaseGlutamic AcidOxygenPyruvate KinaseSuccinates

Identifiers

PMID15792353
OpenAlexW2088059885

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.