Evidence map›Paper›PMID 23380766›Full record

ArticleMolecular psychiatry2013

Corticotropin-releasing hormone exerts direct effects on neuronal progenitor cells: implications for neuroprotection.

Y Koutmani, P K Politis, M Elkouris, G Agrogiannis, M Kemerli, E Patsouris, E Remboutsika, K P Karalis

Open access · bronzeAbstract read
In one paragraph

Article in Molecular psychiatry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 22% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.

  1. Pooled it
  2. Stress, stress systems, and Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Review
  3. Article
  4. Article
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  7. Article
  8. Article
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  10. Article
  11. Review
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  14. Article
  15. Developmental origins of the human hypothalamic-pituitary-adrenal axis.Expert review of endocrinology & metabolism · 2017
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. The Placenta as a Mediator of Stress Effects on Neurodevelopmental Reprogramming.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2016
    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

8 authors at 6 institutions in 2 countries.

Y KoutmaniDepartment of Developmental Biology, Center for Basic Research, Biomedical Research Foundation of the Academy of Athens, Athens, Greece.
P K Politis
M Elkouris
G Agrogiannis
M Kemerli
E Patsouris
E Remboutsika
K P Karalis
Alexander Fleming Biomedical Sciences Research Center · GRAthens State University · USAcademy of Athens · GRAthens Medical Center · GRBiomedical Research Foundation of the Academy of Athens · GRBoston Children's Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neurogenesis during embryonic and adult life is tightly regulated by a network of transcriptional, growth and hormonal factors. Emerging evidence indicates that activation of the stress response, via the associated glucocorticoid increase, reduces neurogenesis and contributes to the development of adult diseases.As corticotrophin-releasing hormone (CRH) or factor is the major mediator of adaptive response to stressors, we sought to investigate its involvement in this process. Accordingly, we found that CRH could reverse the damaging effects of glucocorticoid on neural stem/progenitor cells (NS/PCs), while its genetic deficiency results in compromised proliferation and enhanced apoptosis during neurogenesis. Analyses in fetal and adult mouse brain revealed significant expression of CRH receptors in proliferating neuronal progenitors. Furthermore, by using primary cultures of NS/PCs, we characterized the molecular mechanisms and identified CRH receptor-1 as the receptor mediating the neuroprotective effects of CRH. Finally, we demonstrate the expression of CRH receptors in human fetal brain from early gestational age, in areas of active neuronal proliferation. These observations raise the intriguing possibility for CRH-mediated pharmacological applications in diseases characterized by altered neuronal homeostasis, including depression, dementia, neurodegenerative diseases, brain traumas and obesity.

Indexed as

AnimalsApoptosisBrainCell ProliferationCorticotropin-Releasing HormoneCRF Receptor, Type 1DexamethasoneHumansMiceMice, KnockoutNeurogenesisNeuroprotective AgentsPyrimidinesPyrrolesReceptors, Corticotropin-Releasing HormoneSignal TransductionantalarminCorticotropin-Releasing HormoneCRF Receptor, Type 1DexamethasoneNeuroprotective AgentsPyrimidinesPyrrolesReceptors, Corticotropin-Releasing Hormone

Identifiers

PMID23380766
PMCPMC3578949
OpenAlexW2099489663

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.