Evidence map›Paper›PMID 39196031›Full record

ArticleNature cardiovascular research2024

Cardiac troponin I directly binds and inhibits mitochondrial ATP synthase with a noncanonical role in the post-ischemic heart.

Aly Elezaby, Amanda J Lin, Vijith Vijayan, Suman Pokhrel, Benjamin R Kraemer, Luiz R G Bechara, Isabel Larus, Junhui Sun, Valentina Baena, Zulfeqhar A Syed and 8 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature cardiovascular research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. 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

18 authors.

Aly Elezaby *Department of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA, USA.ORCID http://orcid.org/0000-0001-8389-3200
Amanda J Lin *Department of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA, USA.
Vijith VijayanDepartment of Pediatrics, Division of Critical Care Medicine, Stanford University School of Medicine, Stanford, CA, USA.
Suman PokhrelDepartment of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA, USA.ORCID http://orcid.org/0000-0003-2258-8768
Benjamin R KraemerDepartment of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA, USA.
Luiz R G BecharaDepartment of Anatomy, Institute of Biomedical Sciences, University of Sao Paulo, São Paulo, Brazil.ORCID http://orcid.org/0000-0002-1642-1008
Isabel LarusDepartment of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA, USA.ORCID http://orcid.org/0000-0002-8411-0877
Junhui SunCardiovascular Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Valentina BaenaElectron Microscopy Core, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.ORCID http://orcid.org/0000-0002-6429-439X
Zulfeqhar A SyedElectron Microscopy Core, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Elizabeth MurphyCardiovascular Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Brian GlancySystems Biology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.ORCID http://orcid.org/0000-0002-8571-244X
Nicolai P OstbergDepartment of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA, USA.
Bruno B QueliconiDepartment of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA, USA.
Juliane C CamposDepartment of Anatomy, Institute of Biomedical Sciences, University of Sao Paulo, São Paulo, Brazil.
Julio C B FerreiraDepartment of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA, USA.
Bereketeab HaileselassieDepartment of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA, USA.
Daria Mochly-RosenDepartment of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA, USA. mochly@stanford.edu.ORCID http://orcid.org/0000-0002-6691-8733

Funding

Development and Regulation of the Muscle Mitochondrial ReticulumZIAHL006221 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI GLANCY, BRIAN · 2017 to 2025
$14.7M
Electron Microscopy CoreZICHL005906 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI SYED, ZULFEQHAR · 2009 to 2025
$12.9M
Protein Kinase C Isozymes in Ischemic HeartR01HL052141 · NHLBI · STANFORD UNIVERSITY · PI MOCHLY-ROSEN, DARIA · 1996 to 2021
$8.5M
Dysregulation of Mitochondrial Dynamics in Sepsis R00HD099387 · NICHD · STANFORD UNIVERSITY · PI HAILESELASSIE, BEREKETAB · 2021 to 2023
$747k
Mechanisms of cardiac ischemia-reperfusion injury and cardioprotectionZ01HL002066 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI MURPHY, ELIZABETH · 2008 to 2008
$607k
Dysregulation of Mitochondrial Dynamics in Sepsis Induced Multi-Organ Dysfunction Syndrome (MODS)K99HD099387 · NICHD · STANFORD UNIVERSITY · PI HAILESELASSIE, BEREKETAB · 2020 to 2020
$132k
NO RELEASE MODULATES CORONARY WALL FUNCTIONF33HL009427 · NHLBI · NEW YORK MEDICAL COLLEGE · PI STEWART, JULIAN M · 1996 to 1998
–
American Heart Association (American Heart Association, Inc.) 19POST34380299Fundação de Amparo à Pesquisa do Estado de São Paulo (São Paulo Research Foundation) 2021/09484-7Intramural NIH HHS Z01 HL002066NHLBI NIH HHS R01 HL052141NICHD NIH HHS K99 HD099387U.S. Department of Health & Human Services | NIH | Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) HD099387U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI) HL002066U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI) HL006221U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI) HL052141U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI) HL09427411A1
6 · The paper itself

Abstract

Cardiac troponin I (cTnI) is a key regulator of cardiomyocyte contraction. However, its role in mitochondria is unknown. Here we show that cTnI localized to mitochondria in the heart, inhibited mitochondrial functions when stably expressed in noncardiac cells and increased the opening of the mitochondrial permeability transition pore under oxidative stress. Direct, specific and saturable binding of cTnI to F

Indexed as

Mitochondria, HeartMitochondrial Proton-Translocating ATPasesTroponin IAdenosine TriphosphateAnimalsDisease Models, AnimalHEK293 CellsHumansMaleMiceMice, Inbred C57BLMitochondrial Permeability Transition PoreMyocardial IschemiaMyocardial Reperfusion InjuryOxidative StressProtein BindingAdenosine TriphosphateMitochondrial Permeability Transition PoreMitochondrial Proton-Translocating ATPasesTNNI3 protein, humanTroponin I

Identifiers

PMID39196031
PMCPMC11700703

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.