Evidence map›Paper›PMID 34367466›Full record

ArticleOxidative medicine and cellular longevity2021

Deficiency of ROS-Activated TRPM2 Channel Protects Neurons from Cerebral Ischemia-Reperfusion Injury through Upregulating Autophagy.

Xupang Hu, Lijuan Wu, Xingyu Liu, Yi Zhang, Min Xu, Qiuyuan Fang, Lin Lu, Jianguo Niu, Tarek Mohamed Abd El-Aziz, Lin-Hua Jiang and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

8 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Roles of TRPM channels in glioma.Cancer biology & therapy · 2024
    Review
  3. Article
  4. TLR4 induced TRPM2 mediated neuropathic pain.Frontiers in pharmacology · 2024
    Review
  5. Article
  6. Article
  7. Article
  8. 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

12 authors at 5 institutions in 4 countries.

Xupang Hu *Department of Biophysics, and Department of Neurosurgery of the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310058, China.ORCID https://orcid.org/0000-0002-4982-9552
Lijuan Wu *Department of Biophysics, and Department of Neurosurgery of the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310058, China.ORCID https://orcid.org/0000-0003-2140-9174
Xingyu Liu *Department of Biophysics, and Department of Neurosurgery of the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310058, China.ORCID https://orcid.org/0000-0002-9649-189X
Yi ZhangDepartment of Biophysics, and Department of Neurosurgery of the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310058, China.ORCID https://orcid.org/0000-0001-7321-1202
Min XuDepartment of Biophysics, and Department of Neurosurgery of the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310058, China.ORCID https://orcid.org/0000-0002-9478-8999
Qiuyuan FangDepartment of Biophysics, and Department of Neurosurgery of the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310058, China.ORCID https://orcid.org/0000-0003-1337-4979
Lin LuSchool of Medicine, Zhejiang University City College, Hangzhou 310015, China.ORCID https://orcid.org/0000-0002-7171-9704
Jianguo NiuNingxia Key Laboratory of Craniocerebral Diseases, Ningxia Medical University, Yinchuan 750004, China.ORCID https://orcid.org/0000-0003-2250-3592
Tarek Mohamed Abd El-AzizDepartment of Cellular and Integrative Physiology, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229-3900, USA.ORCID https://orcid.org/0000-0002-3441-9673
Lin-Hua JiangSchool of Biomedical Sciences, Faculty of Biological Sciences, University of Leeds, Leeds, UK.ORCID https://orcid.org/0000-0001-6398-0411
Fangfang LiDepartment of Biophysics, and Department of Neurosurgery of the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310058, China.ORCID https://orcid.org/0000-0001-8943-8831
Wei YangDepartment of Biophysics, and Department of Neurosurgery of the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310058, China.ORCID https://orcid.org/0000-0003-3065-1843
First Affiliated Hospital Zhejiang University · CNNingxia Medical University · CNThe University of Texas Health Science Center at San Antonio · USUniversity of Leeds · GBZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cerebral ischemia-reperfusion (I-R) transiently increased autophagy by producing excessively reactive oxygen species (ROS); on the other hand, activated autophagy would remove ROS-damaged mitochondria and proteins, which led to cell survival. However, the regulation mechanism of autophagy activity during cerebral I-R is still unclear. In this study, we found that deficiency of the TRPM2 channel which is a ROS sensor significantly decreased I-R-induced neuronal damage. I-R transiently increased autophagy activity both

Indexed as

AutophagyAMP-Activated Protein KinasesAnimalsApoptosisBrain IschemiaMiceMice, Inbred C57BLMice, KnockoutNeuronsNeuroprotective AgentsOxidative StressRatsReactive Oxygen SpeciesReperfusion InjurySignal TransductionTOR Serine-Threonine KinasesAMP-Activated Protein KinasesmTOR protein, mouseNeuroprotective AgentsReactive Oxygen SpeciesTOR Serine-Threonine KinasesTRPM2 protein, mouseTRPM Cation Channels

Identifiers

PMID34367466
PMCPMC8337124
OpenAlexW3184948025

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.