Evidence map›Paper›PMID 37062247›Full record

ArticleJournal of molecular and cellular cardiology2023

Btg1 and Btg2 regulate neonatal cardiomyocyte cell cycle arrest.

Nivedhitha Velayutham, Maria Uscategui Calderon, Christina M Alfieri, Stephanie L Padula, Frank N van Leeuwen, Blanca Scheijen, Katherine E Yutzey

Open access · greenAbstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

11 citing papers in PubMed, 10 citations in OpenAlex.

  1. Research progress on BTG2 in non‑tumor diseases (Review).International journal of molecular medicine · 2026
    Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. GDF10 promotes rodent cardiomyocyte maturation during the postnatal period.Journal of molecular and cellular cardiology · 2025
    Article
  8. Review
  9. Article
  10. Article
  11. 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

7 authors at 4 institutions in 2 countries.

Nivedhitha VelayuthamMolecular and Developmental Biology Graduate Program, Division of Developmental Biology, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, OH, USA; The Heart Institute, Division of Molecular Cardiovascular Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Maria Uscategui CalderonMolecular and Developmental Biology Graduate Program, Division of Developmental Biology, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, OH, USA; The Heart Institute, Division of Molecular Cardiovascular Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Christina M AlfieriThe Heart Institute, Division of Molecular Cardiovascular Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Stephanie L PadulaThe Heart Institute, Division of Molecular Cardiovascular Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Frank N van LeeuwenPrincess Máxima Center for Pediatric Oncology, Utrecht, Netherlands.
Blanca ScheijenRadboud University Medical Center, Nijmegen, Netherlands.
Katherine E YutzeyMolecular and Developmental Biology Graduate Program, Division of Developmental Biology, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, OH, USA; The Heart Institute, Division of Molecular Cardiovascular Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA; Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA. Electronic address: Katherine.Yutzey@cchmc.org.
Cincinnati Children's Hospital Medical Center · USPrincess Máxima Center · NLRadboud University Nijmegen · NLUniversity of Cincinnati · US

Funding

Cardiac Fibroblasts in Postnatal Development and Adult Injury ResponseR01HL142217 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI Jeffery D Molkentin, Katherine E Yutzey · 2018 to 2026
$5.9M
Understanding Cardiovascular Disease MechanismsT32HL125204 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI Evangelia G Kranias, Jeffery D Molkentin · 2015 to 2026
$3.4M
Regulatory mechanisms of adult cardiomyocyte proliferationR01HL135848 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI YUTZEY, KATHERINE E · 2017 to 2020
$1.7M
Mechanisms of regulating cardiomyocyte chromatin dynamics and regenerative transitions by Tbx20F32HL159894 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI PADULA, STEPHANIE L · 2021 to 2021
$54k
NHLBI NIH HHS F32 HL159894NHLBI NIH HHS R01 HL135848NHLBI NIH HHS R01 HL142217NHLBI NIH HHS T32 HL125204
6 · The paper itself

Abstract

Rodent cardiomyocytes undergo mitotic arrest in the first postnatal week. Here, we investigate the role of transcriptional co-regulator Btg2 (B-cell translocation gene 2) and functionally-similar homolog Btg1 in postnatal cardiomyocyte cell cycling and maturation. Btg1 and Btg2 (Btg1/2) are expressed in neonatal C57BL/6 mouse left ventricles coincident with cardiomyocyte cell cycle arrest. Btg1/2 constitutive double knockout (DKO) mouse hearts exhibit increased pHH3+ mitotic cardiomyocytes compared to Wildtype at postnatal day (P)7, but not at P30. Similarly, neonatal AAV9-mediated Btg1/2 double knockdown (DKD) mouse hearts exhibit increased EdU+ mitotic cardiomyocytes compared to Scramble AAV9-shRNA controls at P7, but not at P14. In neonatal rat ventricular myocyte (NRVM) cultures, siRNA-mediated Btg1/2 single and double knockdown cohorts showed increased EdU+ cardiomyocytes compared to Scramble siRNA controls, without increase in binucleation or nuclear DNA content. RNAseq analyses of Btg1/2-depleted NRVMs support a role for Btg1/2 in inhibiting cell proliferation, and in modulating reactive oxygen species response pathways, implicated in neonatal cardiomyocyte cell cycle arrest. Together, these data identify Btg1 and Btg2 as novel contributing factors in mammalian cardiomyocyte cell cycle arrest after birth.

Indexed as

Immediate-Early ProteinsTumor Suppressor ProteinsAnimalsCell CycleCell Cycle CheckpointsCell Cycle ProteinsCell ProliferationMammalsMiceMice, Inbred C57BLMyocytes, CardiacNeoplasm ProteinsRatsRNA, Small InterferingBtg1 protein, mouseBtg1 protein, ratBtg2 protein, mouseBTG2 protein, ratCell Cycle ProteinsImmediate-Early ProteinsNeoplasm ProteinsRNA, Small InterferingTumor Suppressor ProteinsBtg1Btg2Cardiac cell cycle regulationCardiomyocyte mitotic arrestNeonatal heart development

Identifiers

PMID37062247
PMCPMC10192094
OpenAlexW4365506154

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.