Evidence map›Paper›PMID 12370307›Full record

ArticleMolecular and cellular biology2002

Targeted disruption of NFATc3, but not NFATc4, reveals an intrinsic defect in calcineurin-mediated cardiac hypertrophic growth.

Benjamin J Wilkins, Leon J De Windt, Orlando F Bueno, Julian C Braz, Betty J Glascock, Thomas F Kimball, Jeffery D Molkentin

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers.

0numbers the graph read from it
0cells of the map it votes in
123citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

123 citing papers in PubMed, 259 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Unlocking the therapeutic potential of the NFAT pathway in kidney diseases.Naunyn-Schmiedeberg's archives of pharmacology · 2025
    Review
  5. Epigenetic Mechanisms in Heart Diseases.Reviews in cardiovascular medicine · 2025
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Inter- and Intracellular Signaling Pathways.Advances in experimental medicine and biology · 2024
    Review
  11. Article
  12. How does NFAT3 regulate the occurrence of cardiac hypertrophy?International journal of cardiology. Heart & vasculature · 2023
    Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. A Review of Calcineurin Biophysics with Implications for Cardiac Physiology.International journal of molecular sciences · 2021
    Review
  20. Review

63 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Benjamin J WilkinsDivision of Molecular Cardiovascular Biology, Department of Pediatrics, Children's Hospital Medical Center, Cincinnati Ohio 45229-3039, USA.
Leon J De Windt
Orlando F Bueno
Julian C Braz
Betty J Glascock
Thomas F Kimball
Jeffery D Molkentin
Cincinnati Children's Hospital Medical Center · US

Funding

TRAINING IN CARDIOVASCULAR BIOLOGYT32HL007382 · NHLBI · UNIVERSITY OF CINCINNATI · PI SCHWARTZ, ARNOLD · 1985 to 2012
$5.9M
ROLE OF CALCINEURIN IN CARDIAC HYPERTROPHYF32HL010336 · NHLBI · CHILDREN'S HOSPITAL MED CTR (CINCINNATI) · PI BUENO, ORLANDO F · 2000 to 2002
$150k
NHLBI NIH HHS 5T32 HL07382NHLBI NIH HHS F32 HL010336NHLBI NIH HHS HL10336NHLBI NIH HHS T32 HL007382
6 · The paper itself

Abstract

A calcineurin-nuclear factor of activated T cells (NFAT) regulatory pathway has been implicated in the control of cardiac hypertrophy, suggesting one mechanism whereby alterations in intracellular calcium handling are linked to the expression of hypertrophy-associated genes. Although recent studies have demonstrated a necessary role for calcineurin as a mediator of cardiac hypertrophy, the potential involvement of NFAT transcription factors as downstream effectors of calcineurin signaling has not been evaluated. Accordingly, mice with targeted disruptions in NFATc3 and NFATc4 genes were characterized. Whereas the loss of NFATc4 did not compromise the ability of the myocardium to undergo hypertrophic growth, NFATc3-null mice demonstrated a significant reduction in calcineurin transgene-induced cardiac hypertrophy at 19 days, 26 days, 6 weeks, 8 weeks, and 10 weeks of age. NFATc3-null mice also demonstrated attenuated pressure overload- and angiotensin II-induced cardiac hypertrophy. These results provide genetic evidence that calcineurin-regulated responses require NFAT effectors in vivo.

Indexed as

MutagenesisAngiotensin IIAnimalsBlotting, WesternCalcineurinCell DivisionCell NucleusDNA-Binding ProteinsFemaleGene TargetingHypertrophyMaleMiceModels, GeneticMutagenesis, Site-DirectedMyocardiumAngiotensin IICalcineurinDNA-Binding ProteinsNfatc3 protein, mouseNfatc4 protein, mouseNFATC Transcription FactorsProtein IsoformsRNA, Messengertranscription factor NF-AT c3Transcription Factors

Identifiers

PMID12370307
PMCPMC135666
OpenAlexW2103445003

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.