Evidence map›Paper›PMID 7831312›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1995

Fibroblast growth factor receptor is required for in vivo cardiac myocyte proliferation at early embryonic stages of heart development.

T Mima, H Ueno, D A Fischman, L T Williams, T Mikawa

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
5.5field-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

47 citing papers in PubMed, 188 citations in OpenAlex.

  1. Epicardium-myocardium crosstalk orchestrates heart development.Frontiers in cell and developmental biology · 2025
    Review
  2. Article
  3. Article
  4. Multi-organ FGF21-FGFR1 signaling in metabolic health and disease.Frontiers in cardiovascular medicine · 2022
    Review
  5. Repression ofScience advances · 2021
    Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Embryonic cardiac chamber maturation: Trabeculation, conduction, and cardiomyocyte proliferation.American journal of medical genetics. Part C, Seminars in medical genetics · 2013
    Review
  16. Epicardial progenitor cells in cardiac development and regeneration.Journal of cardiovascular translational research · 2012
    Review
  17. Article
  18. Epigenetic factors and cardiac development.Cardiovascular research · 2011
    Review
  19. Myocyte proliferation in the developing heart.Developmental dynamics : an official publication of the American Association of Anatomists · 2011
    Review
  20. 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

5 authors at 1 institution in 1 country.

T MimaDepartment of Cell Biology and Anatomy, Cornell University Medical College, New York, NY 10021.
H Ueno
D A Fischman
L T Williams
T Mikawa
Cornell University · US

Funding

MOLECULAR/CELLULAR BIOLOGY OF CARDIOMYOCYTE DEVELOPMENTR01HL045458 · NHLBI · WEILL MEDICAL COLLEGE OF CORNELL UNIV · PI FISCHMAN, DONALD A · 1990 to 2000
$233k
NHLBI NIH HHS HL45458
6 · The paper itself

Abstract

In birds and mammals, cardiac myocytes terminate mitotic activity in the neonatal period and regeneration of cardiac muscle does not occur after myocardial injury in adult hearts. Even embryonic myocytes, which actively proliferate in vivo, quickly lose mitotic activity when placed in cell culture. Several growth factors, including fibroblast growth factor (FGF), have been documented in embryonic hearts and some have been shown to influence myocyte terminal differentiation in culture. However, none of these growth factors have been shown to reactivate cell division in postmitotic myocytes nor have their in vivo functions been defined satisfactorily. To clarify the role of FGF signaling in heart growth, we prepared two retroviral vectors capable of suppressing (i) functions of FGF receptors (FGFRs) with a dominant-negative mutant of receptor type 1 (FGFR1) or (ii) the translation of endogenous FGFR1 by transcribing its antisense RNA. Both vectors inhibited myocyte proliferation and/or survival during the first week of chicken embryonic development but had much less effect after the second week. No apparent alteration of myocyte growth was observed after overexpression of full-length FGFR1. These results suggest that receptor-coupled FGF signaling regulates cardiac myocyte growth during tubular stages of cardiogenesis but that myocyte growth becomes FGF-independent after the second week of embryogenesis.

Indexed as

Receptor Protein-Tyrosine KinasesAnimalsBase SequenceCell SurvivalChick EmbryoGenetic VectorsHeartMitosisMolecular Sequence DataMyocardiumReceptor, Fibroblast Growth Factor, Type 1Receptors, Fibroblast Growth FactorRetroviridaeRNA, AntisenseSignal TransductionTime FactorsReceptor, Fibroblast Growth Factor, Type 1Receptor Protein-Tyrosine KinasesReceptors, Fibroblast Growth FactorRNA, Antisense

Identifiers

PMID7831312
PMCPMC42761
OpenAlexW2084426569

What OpenQuestion holds

Textmetadata
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.