Evidence map›Paper›PMID 30354980›Full record

ArticleStroke2018

Synergistic Interaction Between Zinc and Reactive Oxygen Species Amplifies Ischemic Brain Injury in Rats.

Yongmei Zhao, Feng Yan, Jie Yin, Rong Pan, Wenjuan Shi, Zhifeng Qi, Yalan Fang, Yuyou Huang, Sen Li, Yumin Luo and 2 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Stroke, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.8field-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

38 citing papers in PubMed, 57 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. NOX2-TRPM2 coupling promotes ZnScientific reports · 2024
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  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

12 authors at 2 institutions in 2 countries.

Yongmei ZhaoFrom the Cerebrovascular Diseases Research Institute, Xuanwu Hospital of Capital Medical University, Beijing, China (Y.Z., F.Y., J.Y., W.S., Z.Q., Y.F., Y.H., S.L., Y.L., X.J., K.J.L.).
Feng YanFrom the Cerebrovascular Diseases Research Institute, Xuanwu Hospital of Capital Medical University, Beijing, China (Y.Z., F.Y., J.Y., W.S., Z.Q., Y.F., Y.H., S.L., Y.L., X.J., K.J.L.).
Jie YinFrom the Cerebrovascular Diseases Research Institute, Xuanwu Hospital of Capital Medical University, Beijing, China (Y.Z., F.Y., J.Y., W.S., Z.Q., Y.F., Y.H., S.L., Y.L., X.J., K.J.L.).
Rong PanDepartment of Pharmaceutical Sciences, University of New Mexico, Albuquerque (R.P., K.J.L.).
Wenjuan ShiFrom the Cerebrovascular Diseases Research Institute, Xuanwu Hospital of Capital Medical University, Beijing, China (Y.Z., F.Y., J.Y., W.S., Z.Q., Y.F., Y.H., S.L., Y.L., X.J., K.J.L.).
Zhifeng QiFrom the Cerebrovascular Diseases Research Institute, Xuanwu Hospital of Capital Medical University, Beijing, China (Y.Z., F.Y., J.Y., W.S., Z.Q., Y.F., Y.H., S.L., Y.L., X.J., K.J.L.).
Yalan FangFrom the Cerebrovascular Diseases Research Institute, Xuanwu Hospital of Capital Medical University, Beijing, China (Y.Z., F.Y., J.Y., W.S., Z.Q., Y.F., Y.H., S.L., Y.L., X.J., K.J.L.).
Yuyou HuangFrom the Cerebrovascular Diseases Research Institute, Xuanwu Hospital of Capital Medical University, Beijing, China (Y.Z., F.Y., J.Y., W.S., Z.Q., Y.F., Y.H., S.L., Y.L., X.J., K.J.L.).
Sen LiFrom the Cerebrovascular Diseases Research Institute, Xuanwu Hospital of Capital Medical University, Beijing, China (Y.Z., F.Y., J.Y., W.S., Z.Q., Y.F., Y.H., S.L., Y.L., X.J., K.J.L.).
Yumin LuoFrom the Cerebrovascular Diseases Research Institute, Xuanwu Hospital of Capital Medical University, Beijing, China (Y.Z., F.Y., J.Y., W.S., Z.Q., Y.F., Y.H., S.L., Y.L., X.J., K.J.L.).
Xunming JiFrom the Cerebrovascular Diseases Research Institute, Xuanwu Hospital of Capital Medical University, Beijing, China (Y.Z., F.Y., J.Y., W.S., Z.Q., Y.F., Y.H., S.L., Y.L., X.J., K.J.L.).
Ke Jian LiuFrom the Cerebrovascular Diseases Research Institute, Xuanwu Hospital of Capital Medical University, Beijing, China (Y.Z., F.Y., J.Y., W.S., Z.Q., Y.F., Y.H., S.L., Y.L., X.J., K.J.L.).
Beijing Geriatric Hospital · CNCapital Medical University · CN

Funding

Integrative Program in CNS Pathophysiology ResearchP30GM103400 · NIGMS · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI LIU, KE JIAN · 2012 to 2016
$4.7M
Methamphetamine-induced alterations in brain tissue oxygenationR21DA036721 · NIDA · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI LIU, KE JIAN · 2014 to 2015
$429k
NIDA NIH HHS R21 DA036721NIGMS NIH HHS P30 GM103400
6 · The paper itself

Abstract

Background and Purpose- Although intracellular zinc accumulation has been shown to contribute to neuronal death after cerebral ischemia, the mechanism by which zinc keeps on accumulating to cause severe brain damage remains unclear. Herein the dynamic cause-effect relationships between zinc accumulation and reactive oxygen species (ROS) production during cerebral ischemia/reperfusion are investigated. Methods- Rats were treated with zinc chelator, ROS scavenger, mitochondria-targeted ROS inhibitor, or NADPH oxidase inhibitor during a 90-minute middle cerebral artery occlusion. Cytosolic labile zinc, ROS level, cerebral infarct volume, and neurological functions were assessed after ischemia/reperfusion. Results- Zinc and ROS were colocalized in neurons, leading to neuronal apoptotic death. Chelating zinc reduced ROS production at 6 and 24 hours after reperfusion, whereas eliminating ROS reduced zinc accumulation only at 24 hours. Furthermore, suppression of mitochondrial ROS production reduced the total ROS level and brain damage at 6 hours after reperfusion but did not change zinc accumulation, indicating that ROS is produced mainly from mitochondria during early reperfusion and the initial zinc release is upstream of ROS generation after ischemia. Suppression of NADPH oxidase decreased ROS generation, zinc accumulation, and brain damage only at 24 hours after reperfusion, indicating that the majority of ROS is produced by NADPH oxidase at later reperfusion time. Conclusions- This study provides the direct evidence that there exists a positive feedback loop between zinc accumulation and NADPH oxidase-induced ROS production, which greatly amplifies the damaging effects of both. These findings reveal that different ROS-generating source contributes to ischemia-generated ROS at different time, underscoring the critical importance of spatial and temporal factors in the interaction between ROS and zinc accumulation, and the consequent brain injury, after cerebral ischemia/reperfusion.

Indexed as

AnimalsAntioxidantsApoptosisBiphenyl CompoundsBrainBrain IschemiaChelating AgentsEthylenediaminesInfarction, Middle Cerebral ArteryNADPH OxidasesNeuronsOnium CompoundsOrganometallic CompoundsPramipexoleRatsReactive Oxygen SpeciesAntioxidantsBiphenyl CompoundsChelating AgentsdiphenyliodoniumEthylenediaminesEUK-134NADPH OxidasesN,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamineOnium CompoundsOrganometallic CompoundsPramipexoleReactive Oxygen SpeciesSalicylatesZincbrain ischemiamiddle cerebral arterymitochondriareactive oxygen specieszinc

Identifiers

PMID30354980
PMCPMC6205193
OpenAlexW2890867569

What OpenQuestion holds

Textmetadata
LicenceTDM
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.