Evidence map›Paper›PMID 19064701›Full record

ArticleThe Journal of experimental medicine2008

Control of the adaptive response of the heart to stress via the Notch1 receptor pathway.

Adrien Croquelois, Andrea A Domenighetti, Mohamed Nemir, Mario Lepore, Nathalie Rosenblatt-Velin, Freddy Radtke, Thierry Pedrazzini

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

68 citing papers in PubMed, 128 citations in OpenAlex.

  1. Article
  2. Review
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  6. Article
  7. Article
  8. Regulation of endogenous cardiomyocyte proliferation: The known unknowns.Journal of molecular and cellular cardiology · 2023
    Review
  9. Article
  10. Unlocking cardiomyocyte renewal potential for myocardial regeneration therapy.Journal of molecular and cellular cardiology · 2023
    Review
  11. Article
  12. Article
  13. Article
  14. Signaling pathways and targeted therapy for myocardial infarction.Signal transduction and targeted therapy · 2022
    Review
  15. Review
  16. Review
  17. Review
  18. Review
  19. Article
  20. Triggering of a Dll4-Notch1 loop impairs wound healing in diabetes.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article

8 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.

Adrien CroqueloisDepartment of Medicine, University of Lausanne Medical School, Lausanne, Switzerland.
Andrea A Domenighetti
Mohamed Nemir
Mario Lepore
Nathalie Rosenblatt-Velin
Freddy Radtke
Thierry Pedrazzini
University of Lausanne · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the damaged heart, cardiac adaptation relies primarily on cardiomyocyte hypertrophy. The recent discovery of cardiac stem cells in the postnatal heart, however, suggests that these cells could participate in the response to stress via their capacity to regenerate cardiac tissues. Using models of cardiac hypertrophy and failure, we demonstrate that components of the Notch pathway are up-regulated in the hypertrophic heart. The Notch pathway is an evolutionarily conserved cell-to-cell communication system, which is crucial in many developmental processes. Notch also plays key roles in the regenerative capacity of self-renewing organs. In the heart, Notch1 signaling takes place in cardiomyocytes and in mesenchymal cardiac precursors and is activated secondary to stimulated Jagged1 expression on the surface of cardiomyocytes. Using mice lacking Notch1 expression specifically in the heart, we show that the Notch1 pathway controls pathophysiological cardiac remodeling. In the absence of Notch1, cardiac hypertrophy is exacerbated, fibrosis develops, function is altered, and the mortality rate increases. Therefore, in cardiomyocytes, Notch controls maturation, limits the extent of the hypertrophic response, and may thereby contribute to cell survival. In cardiac precursors, Notch prevents cardiogenic differentiation, favors proliferation, and may facilitate the expansion of a transient amplifying cell compartment.

Indexed as

MyocardiumStress, PhysiologicalAlanineAmyloid Precursor Protein SecretasesAnimalsApoptosisAzepinesCell DifferentiationCells, CulturedGene Expression RegulationHeartMiceMice, KnockoutMice, TransgenicMyocytes, CardiacOligonucleotide Array Sequence AnalysisAlanineAmyloid Precursor Protein SecretasesAzepinesN2-((2S)-2-(3,5-difluorophenyl)-2-hydroxyethanoyl)-N1-((7S)-5-methyl-6-oxo-6,7-dihydro-5H-dibenzo(b,d)azepin-7-yl)-L-alaninamideReceptor, Notch1

Identifiers

PMID19064701
PMCPMC2605223
OpenAlexW2142220620

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.