Evidence map›Paper›PMID 41104836›Full record

ArticleActa physiologica (Oxford, England)2025

Cardiomyocyte-Specific Deletion of Sirtuin 5 Accelerates the Development of Heart Failure Upon Dysregulating Purine Metabolism.

Nikole J Byrne, Christoph Koentges, Katharina Pfeil, Julia C Lueg, Sayan Bakshi, Aleksandre Tarkhnishvili, Ivan Vosko, Johannes Gollmer, Laura C Birkle, Thomas Rathner and 17 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Acta physiologica (Oxford, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

27 authors.

Nikole J ByrneDepartment of Cardiology, University Heart Center Graz, Medical University of Graz, Graz, Austria.
Christoph KoentgesDepartment of Cardiology and Angiology I, Heart Center Freiburg University, Freiburg, Germany.
Katharina PfeilDepartment of Cardiology, University Heart Center Graz, Medical University of Graz, Graz, Austria.
Julia C LuegDepartment of Cardiology and Angiology I, Heart Center Freiburg University, Freiburg, Germany.
Sayan BakshiDivision of Molecular and Cellular Pathology, Department of Pathology, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Aleksandre TarkhnishviliDepartment of Cardiology and Angiology I, Heart Center Freiburg University, Freiburg, Germany.
Ivan VoskoDepartment of Cardiology, University Heart Center Graz, Medical University of Graz, Graz, Austria.ORCID https://orcid.org/0000-0002-6198-888X
Johannes GollmerDepartment of Cardiology, University Heart Center Graz, Medical University of Graz, Graz, Austria.
Laura C BirkleDepartment of Cardiology and Angiology I, Heart Center Freiburg University, Freiburg, Germany.
Thomas RathnerDepartment of Cardiology, University Heart Center Graz, Medical University of Graz, Graz, Austria.
Stephan BirkleDepartment of Cardiology and Angiology I, Heart Center Freiburg University, Freiburg, Germany.
Sibai TangDepartment of Cardiology and Angiology I, Heart Center Freiburg University, Freiburg, Germany.
Clara RauDepartment of Cardiology and Angiology I, Heart Center Freiburg University, Freiburg, Germany.
Michael M HoffmannFaculty of Medicine, University of Freiburg, Freiburg, Germany.ORCID https://orcid.org/0000-0001-8459-6080
Katja E OdeningDepartment of Cardiology and Angiology I, Heart Center Freiburg University, Freiburg, Germany.
Stephen BarnesPharmacology and Toxicology, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Landon Shay WilsonPharmacology and Toxicology, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Senka Ljubojevic-HolzerDepartment of Cardiology, University Heart Center Graz, Medical University of Graz, Graz, Austria.
Markus WallnerDepartment of Cardiology, University Heart Center Graz, Medical University of Graz, Graz, Austria.
Dirk von LewinskiDepartment of Cardiology, University Heart Center Graz, Medical University of Graz, Graz, Austria.
Peter RainerDepartment of Cardiology, University Heart Center Graz, Medical University of Graz, Graz, Austria.
Simon SedejDepartment of Cardiology, University Heart Center Graz, Medical University of Graz, Graz, Austria.
Harald SourijDivision of Endocrinology and Dialectology, Department of Internal Medicine, Medical University of Graz, Graz, Austria.
Christoph BodeDepartment of Cardiology and Angiology I, Heart Center Freiburg University, Freiburg, Germany.
Adam R WendeDivision of Molecular and Cellular Pathology, Department of Pathology, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Andreas ZirlikDepartment of Cardiology, University Heart Center Graz, Medical University of Graz, Graz, Austria.
Heiko BuggerDepartment of Cardiology, University Heart Center Graz, Medical University of Graz, Graz, Austria.

Funding

Novel roles of PDK2 in heart failure: Regulation of mitochondrial nuclear crosstalk via metabolic regulation and histone acetylationR01HL167872 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Adam Raymond Wende · 2023 to 2026
$1.8M
5500 Q-Trap Mass SpectrometerS10RR027822 · NCRR · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BARNES, STEPHEN · 2010 to 2010
$469k
American Heart Association 23PRE1022560Austrian Science Fund 10.55776/STA194Austrian Science Fund 4168-BAustrian Science Fund I3301-B31Austrian Science Fund P-33874 BDeutsche Forschungsgemeinschaft Bu-2126/3-1Deutsche Forschungsgemeinschaft ZI743/7-1Deutsche Forschungsgemeinschaft ZI743/8-1European Research Area Network on Cardiovascular Diseases JCT2017European Research Area Network on Cardiovascular Diseases JCT2018NCRR NIH HHS S10 RR027822NHLBI NIH HHS R01 HL167872NIH HHS HL167872NIH HHS S10 470 RR027822
6 · The paper itself

Abstract

aimSirtuin 5 (SIRT5), a mitochondrial NAD

methodsMice with cardiomyocyte-specific deletion (cSirt5

resultscSirt5-Tg mice had similar cardiac structure and function compared to control mice, whereas cSirt5

conclusionLoss of SIRT5 in cardiomyocytes aggravates cardiac remodeling and dysfunction in response to chronic pressure overload, involving ATP precursor depletion due to transcriptional dysregulation of cardiac purine metabolism.

Indexed as

Heart FailureMyocytes, CardiacPurinesSirtuinsAnimalsMaleMiceMice, Inbred C57BLMice, KnockoutPurinesSIRT5 protein, mouseSirtuinsadenosine kinaseheart failurepurine metabolismSIRT5sirtuin

Identifiers

PMID41104836
PMCPMC12533344

What OpenQuestion holds

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Registered trials

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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.