Evidence map›Paper›PMID 38149324›Full record

ArticleESC heart failure2024

The ratio of cytochrome c oxidase subunit 4 isoform 4I1 and 4I2 mRNA is changed in permanent atrial fibrillation.

Sebastian Vogt, Rabia Ramzan, Pia Cybulski, Annika Rhiel, Petra Weber, Volker Ruppert, Marc Irqsusi, Susanne Rohrbach, Bernd Niemann, Nikolas Mirow and 1 more

Open access · goldAbstract read
In one paragraph

Article in ESC heart failure, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.2field-weighted citation impact, top 18% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

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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 3 institutions in 1 country.

Sebastian VogtCardiovascular Research Lab, Philipps-University Marburg, Marburg, Germany.
Rabia RamzanCardiovascular Research Lab, Philipps-University Marburg, Marburg, Germany.
Pia CybulskiCardiovascular Research Lab, Philipps-University Marburg, Marburg, Germany.
Annika RhielCardiovascular Research Lab, Philipps-University Marburg, Marburg, Germany.
Petra WeberCardiovascular Research Lab, Philipps-University Marburg, Marburg, Germany.
Volker RuppertDepartment of Cardiology, University Hospital of Giessen and Marburg, Marburg, Germany.
Marc IrqsusiDepartment of Cardiac and Vascular Surgery, University Hospital of Giessen and Marburg, Marburg, Germany.
Susanne RohrbachInstitute of Physiology, Justus Liebig University Giessen, Giessen, Germany.
Bernd NiemannDepartment of Cardiac and Vascular Surgery, University Hospital of Giessen and Marburg, Giessen, Germany.
Nikolas MirowDepartment of Cardiac and Vascular Surgery, University Hospital of Giessen and Marburg, Marburg, Germany.
Ardawan J RastanDepartment of Cardiac and Vascular Surgery, University Hospital of Giessen and Marburg, Marburg, Germany.
Universitätsklinikum Gießen und Marburg · DEPhilipps University of Marburg · DEJustus-Liebig-Universität Gießen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsThe conditions of hypoxia are suggested to induce permanent atrial fibrillation (AF). The regulation of COX4I2 and COX4I1 depends on oxygen availability in tissues. A role of COX4I2 in the myocardium of AF patients is supposed for pathogenesis of AF and subsequent alterations in the electron transfer chain (ETC) under hypoxia. METHODS AND

resultsIn vitro, influence of hypoxia on HeLa 53 cells was studied and elevated parts of COX 4I2 were confirmed. Myocardial biopsies were taken ex vivo from the patients' Right Atria with SR (n = 31) and AF (n = 11), respectively. RT- PCR for mRNA expresson, mitochondrial respiration by polarography and the protein content of cytochrome c oxidase (CytOx) subunit 4I1 and CytOx subunit 4I2 by ELISA were studied. Clinical data were correlated to the findings of gene expressions in parallel. Patients with permanent AF had a change in isoform 4I2/4I1 expression along with a decrease of isoform COX 4I1 expression. The 4I2/4I1 ratio of mRNA expression was increased from 0.630 to 1.058 in comparison. However, the protein content of CytOx subunit 4 was much lower in the AF group, whereas the respiration/units enzyme activity in both groups remained the same.

conclusionsThis study describes a possible molecular correlate for the development of AF. Due to the known functional significance of COX 4I2, mitochondrial dysfunction can be assumed as a part of the pathogenesis of AF.

Indexed as

Atrial FibrillationElectron Transport Complex IVRNA, MessengerEnzyme-Linked Immunosorbent AssayFemaleHeLa CellsHumansMaleCOX4I1 protein, humanCOX4I2 protein, humanElectron Transport Complex IVRNA, MessengerCytochrome c oxidase subunit 4Isoform 4I1 and isoform 4I2Mitochondrial respirationPermanent atrial fibrillation

Identifiers

PMID38149324
PMCPMC11098639
OpenAlexW4390273149

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.