Evidence map›Paper›PMID 37972593›Full record

ArticleDevelopmental cell2023

Transcription factor NFYa controls cardiomyocyte metabolism and proliferation during mouse fetal heart development.

Miao Cui, Svetlana Bezprozvannaya, Tian Hao, Abdallah Elnwasany, Luke I Szweda, Ning Liu, Rhonda Bassel-Duby, Eric N Olson

Open access · bronzeAbstract read
In one paragraph

Article in Developmental cell, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

21 citing papers in PubMed, 24 citations in OpenAlex.

  1. NFYB Integrates Hormonal Signals into Tissue Allometry by Promoting Protein Biosynthesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Journal of medicinal chemistry · 2026
    Article
  8. NFS1 Regulates IDH2 to Attenuate Abdominal Aortic Aneurysms via Interacting With SP2.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. NestinJournal of cellular physiology · 2025
    Article
  15. The role(s) of NF-Y in development and differentiation.Cell death and differentiation · 2025
    Review
  16. Review
  17. Article
  18. The molecular mechanisms of cardiac development and related diseases.Signal transduction and targeted therapy · 2024
    Review
  19. Article
  20. LncRNAs in theInternational journal of molecular sciences · 2024
    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

8 authors at 3 institutions in 1 country.

Miao CuiDepartment of Cardiology, Boston Children's Hospital, 300 Longwood Ave, Boston, MA 02115, USA; Department of Genetics, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA. Electronic address: miao_cui@hms.harvard.edu.
Svetlana BezprozvannayaDepartment of Molecular Biology, Hamon Center for Regenerative Science and Medicine and Sen. Paul D. Wellstone Muscular Dystrophy Specialized Research Center, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390, USA.
Tian HaoDepartment of Cardiology, Boston Children's Hospital, 300 Longwood Ave, Boston, MA 02115, USA.
Abdallah ElnwasanyDivision of Cardiology, Department of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390, USA.
Luke I SzwedaDivision of Cardiology, Department of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390, USA.
Ning LiuDepartment of Molecular Biology, Hamon Center for Regenerative Science and Medicine and Sen. Paul D. Wellstone Muscular Dystrophy Specialized Research Center, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390, USA.
Rhonda Bassel-DubyDepartment of Molecular Biology, Hamon Center for Regenerative Science and Medicine and Sen. Paul D. Wellstone Muscular Dystrophy Specialized Research Center, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390, USA.
Eric N OlsonDepartment of Molecular Biology, Hamon Center for Regenerative Science and Medicine and Sen. Paul D. Wellstone Muscular Dystrophy Specialized Research Center, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390, USA. Electronic address: eric.olson@utsouthwestern.edu.
Southwestern Medical Center · USBoston Children's Hospital · USThe University of Texas Southwestern Medical Center · US

Funding

Training CoreP50HD087351 · NICHD · UT SOUTHWESTERN MEDICAL CENTER · PI BASSEL-DUBY, RHONDA, IANNACCONE, SUSAN T · 2020 to 2024
$8.0M
Training CoreU54HD087351 · NICHD · UT SOUTHWESTERN MEDICAL CENTER · PI OLSON, ERIC N · 2015 to 2019
$7.8M
UT Southwestern NORCP30DK127984 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI JONATHAN Charles COHEN · 2022 to 2026
$7.4M
Deciphering the role of a novel micropeptide in cardiac function and dysfunctionR01HL130253 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI BASSEL-DUBY, RHONDA, OLSON, ERIC N · 2016 to 2023
$4.4M
Transcriptional Control of Neonatal Heart RegenerationR01HL157281 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI BASSEL-DUBY, RHONDA, OLSON, ERIC N · 2022 to 2025
$2.2M
Dissecting the cytoprotective role of NRF1 in heart regeneration and repairR00HL153683 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI CUI, MIAO · 2022 to 2024
$747k
Dissecting the cytoprotective role of NRF1 in heart regeneration and repairK99HL153683 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI CUI, MIAO · 2021 to 2022
$190k
NHLBI NIH HHS K99 HL153683NHLBI NIH HHS R00 HL153683NHLBI NIH HHS R01 HL130253NHLBI NIH HHS R01 HL157281NICHD NIH HHS P50 HD087351NICHD NIH HHS U54 HD087351NIDDK NIH HHS P30 DK127984
6 · The paper itself

Abstract

Cardiomyocytes are highly metabolic cells responsible for generating the contractile force in the heart. During fetal development and regeneration, these cells actively divide but lose their proliferative activity in adulthood. The mechanisms that coordinate their metabolism and proliferation are not fully understood. Here, we study the role of the transcription factor NFYa in developing mouse hearts. Loss of NFYa alters cardiomyocyte composition, causing a decrease in immature regenerative cells and an increase in trabecular and mature cardiomyocytes, as identified by spatial and single-cell transcriptome analyses. NFYa-deleted cardiomyocytes exhibited reduced proliferation and impaired mitochondrial metabolism, leading to cardiac growth defects and embryonic death. NFYa, interacting with cofactor SP2, activates genes linking metabolism and proliferation at the transcription level. Our study identifies a nodal role of NFYa in regulating prenatal cardiac growth and a previously unrecognized transcriptional control mechanism of heart metabolism, highlighting the importance of mitochondrial metabolism during heart development and regeneration.

Indexed as

Myocytes, CardiacTranscription FactorsAnimalsCCAAT-Binding FactorCell ProliferationFetal DevelopmentFetal HeartHeartMiceCCAAT-Binding FactorNfya protein, mouseTranscription Factorscardiac metabolismcardiomyocyte proliferationheart developmentnuclear transcription factor Y

Identifiers

PMID37972593
PMCPMC11000264
OpenAlexW4388696185

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.