Evidence map›Paper›PMID 29542681›Full record

ReviewActa pharmacologica Sinica2018

The role of TRPM2 channels in neurons, glial cells and the blood-brain barrier in cerebral ischemia and hypoxia.

Ekaterina Turlova, Zhong-Ping Feng, Hong-Shuo Sun

Open access · hybridAbstract readReview
In one paragraph

Review in Acta pharmacologica Sinica, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

36 citing papers in PubMed, 68 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. The potential role of hypothalamic POMCExperimental & molecular medicine · 2025
    Article
  5. Article
  6. Roles of TRPM channels in glioma.Cancer biology & therapy · 2024
    Review
  7. Article
  8. Article
  9. Review
  10. TLR4 induced TRPM2 mediated neuropathic pain.Frontiers in pharmacology · 2024
    Review
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  12. Review
  13. Review
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  15. Review
  16. Article
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  18. Article
  19. CaInternational journal of molecular sciences · 2022
    Review
  20. 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

3 authors at 2 institutions in 2 countries.

Ekaterina TurlovaDepartments of Surgery.
Zhong-Ping FengDepartments of Physiology.
Hong-Shuo SunDepartments of Surgery.
Czech Academy of Sciences, Institute of Physiology · CZUniversity of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Stroke is one of the major causes of mortality and morbidity worldwide, yet novel therapeutic treatments for this condition are lacking. This review focuses on the roles of the transient receptor potential melastatin 2 (TRPM2) ion channels in cellular damage following hypoxia-ischemia and their potential as a future therapeutic target for stroke. Here, we highlight the complex molecular signaling that takes place in neurons, glial cells and the blood-brain barrier following ischemic insult. We also describe the evidence of TRPM2 involvement in these processes, as shown from numerous in vitro and in vivo studies that utilize genetic and pharmacological approaches. This evidence implicates TRPM2 in a broad range of pathways that take place every stage of cerebral ischemic injury, thus making TRPM2 a promising target for drug development for stroke and other neurodegenerative conditions of the central nervous system.

Indexed as

AnimalsBlood-Brain BarrierCerebral InfarctionHumansHypoxiaNeurogliaNeuronsTRPM Cation ChannelsTRPM2 protein, humanTRPM2 protein, mouseTRPM Cation Channels

Identifiers

PMID29542681
PMCPMC5943904
OpenAlexW2791956573

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.