Evidence map›Paper›PMID 28424623›Full record

ReviewFrontiers in pharmacology2017

Notch Signaling in Ischemic Damage and Fibrosis: Evidence and Clues from the Heart.

Silvia Nistri, Chiara Sassoli, Daniele Bani

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.5field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Heart failure, inflammation and exercise.International journal of biological sciences · 2025
    Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. A perspective on Notch signalling in progression and arrhythmogenesis in familial hypertrophic and dilated cardiomyopathies.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023
    Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Role of the microRNA-29 family in myocardial fibrosis.Journal of physiology and biochemistry · 2021
    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

3 authors at 1 institution in 1 country.

Silvia NistriResearch Unit of Histology and Embryology, Department of Experimental and Clinical Medicine, University of FlorenceFlorence, Italy.
Chiara SassoliDepartment of Experimental and Clinical Medicine, Section of Anatomy and Histology, University of FlorenceFlorence, Italy.
Daniele BaniResearch Unit of Histology and Embryology, Department of Experimental and Clinical Medicine, University of FlorenceFlorence, Italy.
University of Florence · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Notch signaling is a major intercellular coordination mechanism highly conserved throughout evolution. In vertebrates, Notch signaling is physiologically involved in embryo development, including mesenchymal cell commitment, formation of heart tissues and angiogenesis. In post-natal life, Notch signaling is maintained as a key mechanism of cell-cell communication and its dysregulations have been found in pathological conditions such as ischemic and fibrotic diseases. In the heart, Notch takes part in the protective response to ischemia, being involved in pre- and post-conditioning, reduction of reperfusion-induced oxidative stress and myocardial damage, and cardiomyogenesis. Conceivably, the cardioprotective effects of Notch may depend on neo-angiogenesis, thus blunting lethal myocardial ischemia, as well as on direct stimulation of cardiac cells to increase their resistance to injury. Another post-developmental adaptation of Notch signaling is fibrosis: being involved in the orientation of mesenchymal cell fate, Notch can modulate the differentiation of pro-fibrotic myofibroblasts, e.g., by reducing the effects of the profibrotic cytokine TGF-β. In conclusion, Notch can regulate the interactions between heart muscle and stromal cells and switch cardiac repair from a pro-fibrotic default pathway to a pro-cardiogenic one. These features make Notch signaling a suitable target for new cardiotropic therapies.

Indexed as

cardiac preconditioningfibrosisheartischemia-reperfusionNotch

Identifiers

PMID28424623
PMCPMC5381357
OpenAlexW2604752830

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.