Evidence map›Paper›PMID 24603536›Full record

ReviewInternational journal of molecular sciences2014

Mitochondria in the center of human eosinophil apoptosis and survival.

Pinja Ilmarinen, Eeva Moilanen, Hannu Kankaanranta

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

23 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
  2. Targeting mitochondrial function as a potential therapeutic approach for allergic asthma.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
  3. Article
  4. Unraveling the Therapeutic Potential ofCurrent pharmaceutical design · 2025
    Article
  5. Review
  6. Review
  7. Mitochondria signaling pathways in allergic asthma.Journal of investigative medicine : the official publication of the American Federation for Clinical Research · 2022
    Review
  8. Review
  9. Article
  10. Syndromic Deafness GeneFrontiers in cell and developmental biology · 2021
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. TNFα induces CaJournal of experimental & clinical cancer research : CR · 2018
    Article
  16. Review
  17. Article
  18. Article
  19. Article
  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 3 institutions in 1 country.

Pinja IlmarinenThe Immunopharmacology Research Group, University of Tampere School of Medicine and Tampere University Hospital, Tampere FI-33014, Finland. pinja.ilmarinen@uta.fi.
Eeva MoilanenThe Immunopharmacology Research Group, University of Tampere School of Medicine and Tampere University Hospital, Tampere FI-33014, Finland. eeva.moilanen@uta.fi.
Hannu KankaanrantaThe Immunopharmacology Research Group, University of Tampere School of Medicine and Tampere University Hospital, Tampere FI-33014, Finland. hannu.kankaanranta@epshp.fi.
Seinäjoki University of Applied Sciences · FITampere University · FITampere University · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Eosinophils are abundantly present in most phenotypes of asthma and they contribute to the maintenance and exacerbations of the disease. Regulators of eosinophil longevity play critical roles in determining whether eosinophils accumulate into the airways of asthmatics. Several cytokines enhance eosinophil survival promoting eosinophilic airway inflammation while for example glucocorticoids, the most important anti-inflammatory drugs used to treat asthma, promote the intrinsic pathway of eosinophil apoptosis and by this mechanism contribute to the resolution of eosinophilic airway inflammation. Mitochondria seem to play central roles in both intrinsic mitochondrion-centered and extrinsic receptor-mediated pathways of apoptosis in eosinophils. Mitochondria may also be important for survival signalling. In addition to glucocorticoids, another important agent that regulates human eosinophil longevity via mitochondrial route is nitric oxide, which is present in increased amounts in the airways of asthmatics. Nitric oxide seems to be able to trigger both survival and apoptosis in eosinophils. This review discusses the current evidence of the mechanisms of induced eosinophil apoptosis and survival focusing on the role of mitochondria and clinically relevant stimulants, such as glucocorticoids and nitric oxide.

Indexed as

ApoptosisCell SurvivalEosinophilsGlucocorticoidsHumansMitochondriaModels, BiologicalNitric OxideReactive Oxygen SpeciesSignal TransductionGlucocorticoidsNitric OxideReactive Oxygen Species

Identifiers

PMID24603536
PMCPMC3975377
OpenAlexW2042357340

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.