Evidence map›Paper›PMID 38012305›Full record

ArticleNature biomedical engineering2024

Tachycardia-induced metabolic rewiring as a driver of contractile dysfunction.

Chengyi Tu, Arianne Caudal, Yu Liu, Nikoloz Gorgodze, Hao Zhang, Chi Keung Lam, Yuqin Dai, Angela Zhang, Alexa Wnorowski, Matthew A Wu and 8 more

Open access · greenAbstract read
In one paragraph

Article in Nature biomedical engineering, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

23 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
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  6. Beta-Adrenergic Stimulation andbioRxiv : the preprint server for biology · 2026
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  11. Review
  12. Cardiac fibrosis: from mechanisms and models to medicines.Trends in pharmacological sciences · 2025
    Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. Conductive Microfibers Improve Stem Cell-Derived Cardiac Spheroid Maturation.Journal of biomedical materials research. Part A · 2025
    Article
  20. 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

18 authors at 5 institutions in 2 countries.

Chengyi TuStanford Cardiovascular Institute, Stanford University, Stanford, CA, USA.
Arianne CaudalStanford Cardiovascular Institute, Stanford University, Stanford, CA, USA.
Yu LiuStanford Cardiovascular Institute, Stanford University, Stanford, CA, USA.
Nikoloz GorgodzeAging + Cardiovascular Discovery Center, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, USA.
Hao ZhangStanford Cardiovascular Institute, Stanford University, Stanford, CA, USA.
Chi Keung LamStanford Cardiovascular Institute, Stanford University, Stanford, CA, USA.
Yuqin DaiSarafan ChEM-H, Stanford University, Stanford, CA, USA.
Angela ZhangStanford Cardiovascular Institute, Stanford University, Stanford, CA, USA.ORCID http://orcid.org/0000-0003-0906-6770
Alexa WnorowskiStanford Cardiovascular Institute, Stanford University, Stanford, CA, USA.
Matthew A WuStanford Cardiovascular Institute, Stanford University, Stanford, CA, USA.
Huaxiao YangStanford Cardiovascular Institute, Stanford University, Stanford, CA, USA.
Oscar J AbilezStanford Cardiovascular Institute, Stanford University, Stanford, CA, USA.ORCID http://orcid.org/0000-0002-9991-400X
Xuchao LyuDepartment of Pathology, Stanford University, Stanford, CA, USA.ORCID http://orcid.org/0000-0003-1967-3902
Sanjiv M NarayanDepartment of Medicine, Stanford University, Stanford, CA, USA.ORCID http://orcid.org/0000-0001-7552-5053
Luisa MestroniHuman Medical Genetics and Genomics, University of Colorado, Aurora, CO, USA.
Matthew R G TaylorHuman Medical Genetics and Genomics, University of Colorado, Aurora, CO, USA.
Fabio A RecchiaAging + Cardiovascular Discovery Center, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, USA.
Joseph C WuStanford Cardiovascular Institute, Stanford University, Stanford, CA, USA. joewu@stanford.edu.ORCID http://orcid.org/0000-0002-6068-8041
Cardiovascular Institute of the South · USStanford University · USUniversity of Colorado Anschutz Medical Campus · USScuola Superiore Sant'Anna · ITTemple University · US

Funding

Project 3 (Mercola)P01HL141084 · NHLBI · STANFORD UNIVERSITY · PI MARK MERCOLA · 2019 to 2026
$21.1M
Human Induced Pluripotent Stem Cells for Cardiovascular Disease ModelingR01HL113006 · NHLBI · STANFORD UNIVERSITY · PI WU, JOSEPH C. · 2012 to 2025
$6.8M
Human iPSCs for Elucidating Intercellular Crosstalk Signaling in Dilated CardiomyopathyR01HL141371 · NHLBI · STANFORD UNIVERSITY · PI WONG, WING H., WU, JOSEPH C. · 2018 to 2025
$6.2M
Elucidating Anthracycline-Induced Cell Type-Specific Cardiovascular Toxicity with CRISPRi/a ScreensR01HL150693 · NHLBI · STANFORD UNIVERSITY · PI Ronglih Liao, Joseph C. Wu · 2021 to 2026
$4.1M
Targeting Ketone Metabolism as a Novel Heart Failure TherapyR01HL151345 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI KELLY, DANIEL PATRICK, RECCHIA, FABIO A · 2020 to 2023
$3.2M
Engineering Cardiac spheroids to study LaminopathiesR01HL164634 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI Luisa Mestroni, Matthew R Taylor · 2023 to 2026
$2.8M
Elucidating ECM Signaling in Cardiac Organoids with Machine Learning and Single-cell MultiomicsR01HL163680 · NHLBI · STANFORD UNIVERSITY · PI RAJADAS, JAYAKUMAR, WONG, WING H. · 2022 to 2025
$2.5M
Optogenetic Engineered Heart Muscle for Disease ModelingK01HL130608 · NHLBI · STANFORD UNIVERSITY · PI ABILEZ, OSCAR JOHN · 2016 to 2020
$862k
Tachycardia-induced Metabolic Remodeling Drives Cardiac DysfunctionK99HL164962 · NHLBI · STANFORD UNIVERSITY · PI TU, CHENGYI · 2023 to 2024
$303k
NHLBI NIH HHS K01 HL130608NHLBI NIH HHS K99 HL164962NHLBI NIH HHS P01 HL141084NHLBI NIH HHS R01 HL113006NHLBI NIH HHS R01 HL141371NHLBI NIH HHS R01 HL150693NHLBI NIH HHS R01 HL151345NHLBI NIH HHS R01 HL163680NHLBI NIH HHS R01 HL164634
6 · The paper itself

Abstract

Prolonged tachycardia-a risk factor for cardiovascular morbidity and mortality-can induce cardiomyopathy in the absence of structural disease in the heart. Here, by leveraging human patient data, a canine model of tachycardia and engineered heart tissue generated from human induced pluripotent stem cells, we show that metabolic rewiring during tachycardia drives contractile dysfunction by promoting tissue hypoxia, elevated glucose utilization and the suppression of oxidative phosphorylation. Mechanistically, a metabolic shift towards anaerobic glycolysis disrupts the redox balance of nicotinamide adenine dinucleotide (NAD), resulting in increased global protein acetylation (and in particular the acetylation of sarcoplasmic/endoplasmic reticulum Ca

Indexed as

Induced Pluripotent Stem CellsNADTachycardiaAnimalsCardiomyopathiesDogsGlucoseGlycolysisHumansMaleMyocardial ContractionMyocytes, CardiacOxidation-ReductionOxidative PhosphorylationSarcoplasmic Reticulum Calcium-Transporting ATPasesTissue EngineeringGlucoseNADSarcoplasmic Reticulum Calcium-Transporting ATPases

Identifiers

PMID38012305
PMCPMC11088531
OpenAlexW4389046135

What OpenQuestion holds

Textmetadata
LicenceTDM
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.