Evidence map›Paper›PMID 41366320›Full record

ArticleBMC cardiovascular disorders2025

Integrated bioinformatic and in vivo analysis confirms the cardioprotective role of OPA1.

Claire Fong-McMaster, Serena M Pulente, Luke S Kennedy, Tyler K T Smith, Stephanie Myers, Michel N Kanaan, Charbel Y Karam, Matthew Cope, Michelle M Levesque, Ella McIlroy and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC cardiovascular disorders, 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

16 authors.

Claire Fong-McMasterDepartment of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, ON, Canada.
Serena M PulenteDepartment of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, ON, Canada.
Luke S KennedyDepartment of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, ON, Canada.
Tyler K T SmithDepartment of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, ON, Canada.
Stephanie MyersDepartment of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, ON, Canada.
Michel N KanaanDepartment of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, ON, Canada.
Charbel Y KaramDepartment of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, ON, Canada.
Matthew CopeDepartment of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, ON, Canada.
Michelle M LevesqueDepartment of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, ON, Canada.
Ella McIlroyDepartment of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, ON, Canada.
Ilka Lorenzen-SchmidtUniversity of Ottawa Heart Institute, Ottawa, ON, Canada.
Craig J GoergenWeldon School of Biomedical Engineering, Purdue University, West Lafayette, IN, USA.
Morgan D FullertonDepartment of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, ON, Canada.
Miroslava Cuperlovic-CulfDepartment of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, ON, Canada.
Erin E MulvihillDepartment of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, ON, Canada. emulvihi@uottawa.ca.
Mary-Ellen HarperDepartment of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, ON, Canada. mharper@uottawa.ca.

Funding

CIHR 143278CIHR 148634CIHR 186076Heart and Stroke Foundation of Canada Grant-in-AidHeart and Stroke Foundation of Canada New Investigator Award
6 · The paper itself

Abstract

backgroundOPA1 is an inner mitochondrial membrane protein that mediates diverse signaling processes. OPA1 is important for cardiac function and protects against cardiac insults such as ischemia/reperfusion injury. We sought to further assess OPA1 in cardiac pathologies, hypothesizing that OPA1 will function in a protective manner in chronic heart failure.

methodsIntegrated analyses of publicly available histological and transcriptomic data were used to identify functional associations between OPA1 and other genes of interest. To experimentally assess these associations, mice with a 1.5-fold whole body OPA1 overexpression (OPA1-OE) were subjected to a modified transverse aortic constriction surgery and underwent 2-dimensional and 4-dimensional echocardiography along with molecular analyses including high-resolution respirometry, enzymatic activities, flow cytometry and transcript level analyses.

resultsBioinformatic analyses of histological and transcript data from the GTEx database indicated that OPA1 expression levels vary in the human heart, where elevated OPA1 transcript levels were associated with fatty acid, branch chain amino acid and cardiac contractile gene signatures. These functional associations were further supported by in vivo findings showing that OPA1-OE mice displayed improved 2D ejection fraction, end systolic volume, end diastolic volume and 4D cardiac functional parameters including global peak circumferential and surface area strain compared to WT mice. As well, OPA1-OE mice displayed sustained transcript levels of fatty acid, branch chain amino acid and contractile markers and no induction of fibrotic transcript markers.

conclusionThese results further demonstrate the important role of OPA1 in supporting optimal cardiac function and highlight potentially protective contractile and metabolic signaling pathways.

Indexed as

Computational BiologyGTP PhosphohydrolasesHeart FailureMyocardiumMyocytes, CardiacVentricular Function, LeftAnimalsDatabases, GeneticDisease Models, AnimalEnergy MetabolismGene Expression ProfilingHumansMaleMiceMice, Inbred C57BLMice, TransgenicGTP PhosphohydrolasesOPA1 protein, humanOpa1 protein, mouse4-dimensional echocardiographyHeart failureMitochondriaMitochondrial fusionOptic atrophy protein-1

Identifiers

PMID41366320
PMCPMC12802031

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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.