Evidence map›Paper›PMID 31827131›Full record

ArticleScientific reports2019

Defined factors to reactivate cell cycle activity in adult mouse cardiomyocytes.

Justin Judd, Jonathan Lovas, Guo N Huang

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

12 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. The E2F family: a ray of dawn in cardiomyopathy.Molecular and cellular biochemistry · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Repression ofScience advances · 2021
    Article
  9. Review
  10. Review
  11. Article
  12. 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

3 authors at 1 institution in 1 country.

Justin JuddCardiovascular Research Institute, University of California, San Francisco, San Francisco, CA, 94158, USA.
Jonathan LovasCardiovascular Research Institute, University of California, San Francisco, San Francisco, CA, 94158, USA.
Guo N HuangCardiovascular Research Institute, University of California, San Francisco, San Francisco, CA, 94158, USA. Guo.Huang@ucsf.edu.
University of California, San Francisco · US

Funding

MOLECULAR AND CELLULAR BASIS OF CARDIOVASCULAR DISEASET32HL007731 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Brian L Black · 1992 to 2026
$12.4M
Molecular control of cardiac regenerative potentialR01HL138456 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Guo Huang · 2018 to 2026
$5.1M
NHLBI NIH HHS R01 HL138456NHLBI NIH HHS T32 HL007731U.S. Department of Health & Human Services | National Institutes of Health (NIH) T32HL007731
6 · The paper itself

Abstract

Adult mammalian cardiomyocytes exit the cell cycle during the neonatal period, commensurate with the loss of regenerative capacity in adult mammalian hearts. We established conditions for long-term culture of adult mouse cardiomyocytes that are genetically labeled with fluorescence. This technique permits reliable analyses of proliferation of pre-existing cardiomyocytes without complications from cardiomyocyte marker expression loss due to dedifferentiation or significant contribution from cardiac progenitor cell expansion and differentiation in culture. Using this system, we took a candidate gene approach to screen for fetal-specific proliferative gene programs that can induce proliferation of adult mouse cardiomyocytes. Using pooled gene delivery and subtractive gene elimination, we identified a novel functional interaction between E2f Transcription Factor 2 (E2f2) and Brain Expressed X-Linked (Bex)/Transcription elongation factor A-like (Tceal) superfamily members Bex1 and Tceal8. Specifically, Bex1 and Tceal8 both preserved cell viability during E2f2-induced cell cycle re-entry. Although Tceal8 inhibited E2f2-induced S-phase re-entry, Bex1 facilitated DNA synthesis while inhibiting cell death. In sum, our study provides a valuable method for adult cardiomyocyte proliferation research and suggests that Bex family proteins may function in modulating cell proliferation and death decisions during cardiomyocyte development and maturation.

Indexed as

Cell DedifferentiationAnimalsCell CycleCell ProliferationDNA ReplicationE2F2 Transcription FactorMiceMyocytes, CardiacNerve Tissue ProteinsSignal TransductionBex1 protein, mouseE2f2 protein, mouseE2F2 Transcription FactorNerve Tissue Proteins

Identifiers

PMID31827131
PMCPMC6906479
OpenAlexW2996574246

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.