Evidence map›Paper›PMID 32825703›Full record

ArticleInternational journal of molecular sciences2020

Transient Receptor Potential Melastatin 2 (TRPM2) Inhibition by Antioxidant,

Dae Ki Hong, A Ra Kho, Song Hee Lee, Jeong Hyun Jeong, Beom Seok Kang, Dong Hyeon Kang, Min Kyu Park, Kyoung-Ha Park, Man-Sup Lim, Bo Young Choi and 1 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.0field-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

15 citing papers in PubMed, 20 citations in OpenAlex.

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  11. Review
  12. Protective Role of Glutathione in the Hippocampus after Brain Ischemia.International journal of molecular sciences · 2021
    Review
  13. Neuroprotection: Rescue from Neuronal Death in the Brain.International journal of molecular sciences · 2021
    Article
  14. Article
  15. 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

11 authors at 2 institutions in 1 country.

Dae Ki HongDepartment of Physiology, College of Medicine, Hallym University, Chuncheon 24252, Korea.
A Ra KhoDepartment of Physiology, College of Medicine, Hallym University, Chuncheon 24252, Korea.
Song Hee LeeDepartment of Physiology, College of Medicine, Hallym University, Chuncheon 24252, Korea.
Jeong Hyun JeongDepartment of Physiology, College of Medicine, Hallym University, Chuncheon 24252, Korea.
Beom Seok KangDepartment of Physiology, College of Medicine, Hallym University, Chuncheon 24252, Korea.
Dong Hyeon KangDepartment of Medical Science, College of Medicine, Hallym University, Chuncheon 24252, Korea.
Min Kyu ParkDepartment of Physiology, College of Medicine, Hallym University, Chuncheon 24252, Korea.
Kyoung-Ha ParkDivision of Cardiovascular Diseases, Hallym University Medical Center, Anyang 14068, Korea.
Man-Sup LimDepartment of Medical Education, College of Medicine, Hallym University, Chuncheon 24252, Korea.
Bo Young ChoiDepartment of Physiology, College of Medicine, Hallym University, Chuncheon 24252, Korea.
Sang Won SuhDepartment of Physiology, College of Medicine, Hallym University, Chuncheon 24252, Korea.
Hallym University · KRHallym University Medical Center · KR

Funding

National Research Foundation of Korea 2017M3C7A1028937National Research Foundation of Korea 2019R1A2C4004912National Research Foundation of Korea 2019R1A6A3A13093671National Research Foundation of Korea 2020R1A2C2008480
6 · The paper itself

Abstract

A variety of pathogenic mechanisms, such as cytoplasmic calcium/zinc influx, reactive oxygen species production, and ionic imbalance, have been suggested to play a role in cerebral ischemia induced neurodegeneration. During the ischemic state that occurs after stroke or heart attack, it is observed that vesicular zinc can be released into the synaptic cleft, and then translocated into the cytoplasm via various cation channels. Transient receptor potential melastatin 2 (TRPM2) is highly distributed in the central nervous system and has high sensitivity to oxidative damage. Several previous studies have shown that TRPM2 channel activation contributes to neuroinflammation and neurodegeneration cascades. Therefore, we examined whether anti-oxidant treatment, such as with

Indexed as

AcetylcysteineAnimalsAntioxidantsBrain IschemiaGlutathioneHippocampusLipid PeroxidationNeurogliaNeuronsRatsTRPM Cation ChannelsZincAcetylcysteineAntioxidantsGlutathioneTrpm2 protein, ratTRPM Cation ChannelsZincglobal cerebral ischemiaN-acetyl-l-cysteineneurodegenerationtransient receptor potential melastatin 2zinc

Identifiers

PMID32825703
PMCPMC7504640
OpenAlexW3080611215

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.