Evidence map›Paper›PMID 42073991›Full record

ArticleInternational journal of molecular sciences2026

Coenzyme Q

Filip Klaučo, Iveta Šimková, Zuzana Sumbalová, Tereza Hlavatá, Monika Kaldarárová, Guillermo López-Lluch, Anna Gvozdjáková

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

7 authors.

Filip KlaučoDepartment of Cardiology and Angiology, Adult Congenital Heart Disease Division, Slovak Medical University, National Institute of Cardiovascular Diseases, Pod Krásnou Hôrkou 1, 833 48 Bratislava, Slovakia.ORCID 0009-0007-1964-7612
Iveta ŠimkováDepartment of Cardiology and Angiology, Adult Congenital Heart Disease Division, Slovak Medical University, National Institute of Cardiovascular Diseases, Pod Krásnou Hôrkou 1, 833 48 Bratislava, Slovakia.ORCID 0000-0002-6051-2724
Zuzana SumbalováInstitute of Medical Chemistry, Biochemistry and Clinical Biochemistry, Faculty of Medicine, Comenius University in Bratislava, Sasinkova 2, 811 08 Bratislava, Slovakia.ORCID 0000-0001-9454-6255
Tereza HlavatáDepartment of Cardiology and Angiology, Adult Congenital Heart Disease Division, Slovak Medical University, National Institute of Cardiovascular Diseases, Pod Krásnou Hôrkou 1, 833 48 Bratislava, Slovakia.
Monika KaldarárováDepartment of Cardiology and Angiology, Adult Congenital Heart Disease Division, Slovak Medical University, National Institute of Cardiovascular Diseases, Pod Krásnou Hôrkou 1, 833 48 Bratislava, Slovakia.
Guillermo López-LluchDepartment of Physiology, Anatomy and Cell Biology, Andalusian Centre of Developmental Biology (CABD-CSIC-JA), Universidad Pablo de Olavide, Carretera de Utrera Km. 1, 410 13 Seville, Spain.ORCID 0000-0001-9830-8502
Anna GvozdjákováInstitute of Medical Chemistry, Biochemistry and Clinical Biochemistry, Faculty of Medicine, Comenius University in Bratislava, Sasinkova 2, 811 08 Bratislava, Slovakia.ORCID 0000-0002-5139-9213

Funding

Slovak Medical University VG RSZU620/2024
6 · The paper itself

Abstract

Congenital heart diseases (CHDs) are characterized by profound metabolic remodeling of mitochondrial pathways. However, data regarding mitochondrial respiration, oxidative phosphorylation (OXPHOS), and fatty acid oxidation (FAO) in patients with Ebstein anomaly (EA) are currently unavailable. This study evaluated 14 EA patients and 18 healthy volunteers. In accordance with the 2020 ESC guidelines, patients were stratified into two cohorts: EA-0 (patients currently without an indication for intervention) and EA-1 (patients meeting Class Ia or IIb indications for surgical intervention). Platelet OXPHOS and FAO parameters were determined simultaneously via high-resolution respirometry. CI-linked LEAK respiration (substrates: pyruvate and malate) and FAO-linked LEAK respiration (substrates: octanoylcarnitine and malate) were significantly elevated in EA patients. Furthemore, the EA-1 group showed significantly lower coenzyme Q

Indexed as

Ebstein AnomalyHeart FailureMetabolism, Inborn ErrorsMitochondriaMitochondrial DiseasesUbiquinoneAdolescentAdultAtaxiaBiomarkersBlood PlateletsCell RespirationChildChild, PreschoolEnergy MetabolismFatty AcidsBiomarkerscoenzyme Q10Fatty AcidsUbiquinonecoenzyme Q10Ebstein anomalyFAOmitochondrial bioenergeticsOXPHOSpersonalized treatmentplateletsreprogrammingγ-tocopherol

Identifiers

PMID42073991
PMCPMC13116391

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.