Evidence map›Paper›PMID 27694219›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2016

FOXO3a regulates BNIP3 and modulates mitochondrial calcium, dynamics, and function in cardiac stress.

Antoine H Chaanine, Erik Kohlbrenner, Scott I Gamb, Adam J Guenzel, Katherine Klaus, Ahmed U Fayyaz, K Sreekumaran Nair, Roger J Hajjar, Margaret M Redfield

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

59 citing papers in PubMed, 97 citations in OpenAlex.

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  15. Mitochondrial Dysfunction in the Cardio-Renal Axis.International journal of molecular sciences · 2023
    Review
  16. Review
  17. miRNAs in Uremic Cardiomyopathy: A Comprehensive Review.International journal of molecular sciences · 2023
    Review
  18. Article
  19. Review
  20. Mitochondrial quality control in health and cardiovascular diseases.Frontiers in cell and developmental biology · 2023
    Review
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

9 authors at 3 institutions in 1 country.

Antoine H ChaanineDivision of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota.ORCID 0000-0002-9603-7849
Erik KohlbrennerDivision of Cardiovascular Diseases, Mount Sinai School of Medicine, New York, New York.
Scott I GambMicroscopy and Cell Analysis Core, Department of Biochemistry and Cell Biology, Mayo Clinic, Rochester, Minnesota; and.
Adam J GuenzelDivision of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota.
Katherine KlausDivision of Endocrinology, Mayo Clinic, Rochester, Minnesota.
Ahmed U FayyazDivision of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota.
K Sreekumaran NairDivision of Endocrinology, Mayo Clinic, Rochester, Minnesota.
Roger J HajjarDivision of Cardiovascular Diseases, Mount Sinai School of Medicine, New York, New York.
Margaret M RedfieldDivision of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota; redfield.margaret@mayo.edu.
Mayo Clinic · USIcahn School of Medicine at Mount Sinai · USMayo Clinic in Florida · US

Funding

Recruitment and Phenotyping CoreP01HL076611 · NHLBI · MAYO CLINIC ROCHESTER · PI BURNETT, JOHN C · 2005 to 2015
$19.6M
Treatment of Diastolic Heart Failure via AAV-9 Mediated Gene TransferR01HL105418 · NHLBI · MAYO CLINIC ROCHESTER · PI REDFIELD, MARGARET M · 2012 to 2015
$1.5M
NHLBI NIH HHS P01 HL076611NHLBI NIH HHS R01 HL105418
6 · The paper itself

Abstract

The forkhead box O3a (FOXO3a) transcription factor has been shown to regulate glucose metabolism, muscle atrophy, and cell death in postmitotic cells. Its role in regulation of mitochondrial and myocardial function is not well studied. Based on previous work, we hypothesized that FOXO3a, through BCL2/adenovirus E1B 19-kDa protein-interacting protein 3 (BNIP3), modulates mitochondrial morphology and function in heart failure (HF). We modulated the FOXO3a-BNIP3 pathway in normal and phenylephrine (PE)-stressed adult cardiomyocytes (ACM) in vitro and developed a cardiotropic adeno-associated virus serotype 9 encoding dominant-negative FOXO3a (AAV9.dn-FX3a) for gene delivery in a rat model of HF with preserved ejection fraction (HFpEF). We found that FOXO3a upregulates BNIP3 expression in normal and PE-stressed ACM, with subsequent increases in mitochondrial Ca

Indexed as

AnimalsBlotting, WesternCalciumCalcium-Binding ProteinsCell SurvivalCitrate (si)-SynthaseDisease Models, AnimalDynaminsEchocardiographyElectron Transport Complex IVEndoplasmic ReticulumFluorescent Antibody TechniqueForkhead Box Protein O3Heart FailureIn Vitro TechniquesMaleBNIP3 protein, ratCalciumCalcium-Binding ProteinsCitrate (si)-SynthaseDnm1l protein, ratDynaminsElectron Transport Complex IVForkhead Box Protein O3FOXO3 protein, ratMembrane ProteinsMitochondrial ProteinsPhenylephrinePhospholambanSympathomimeticsapoptosisBNIP3calcium regulationFOXO3aheart failure

Identifiers

PMID27694219
PMCPMC5206339
OpenAlexW2527459561

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.