Evidence map›Paper›PMID 36184790›Full record

ArticleCNS neuroscience & therapeutics2022

Ferroptosis contributes to hypoxic-ischemic brain injury in neonatal rats: Role of the SIRT1/Nrf2/GPx4 signaling pathway.

Chang Li, Ziyi Wu, Hang Xue, Qiushi Gao, Yahan Zhang, Changming Wang, Ping Zhao

Open access · goldAbstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 2 pooled it
10.2field-weighted citation impact, top 1% 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

66 citing papers in PubMed, 2 syntheses or guidelines pooled it, 116 citations in OpenAlex.

  1. Pooled it
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6 more citing papers are in PubMed but not listed here.

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

7 authors at 2 institutions in 1 country.

Chang LiDepartment of Anesthesiology, Shengjing Hospital of China Medical University, Shenyang, Liaoning, China.ORCID 0000-0003-1413-0896
Ziyi WuDepartment of Anesthesiology, Shengjing Hospital of China Medical University, Shenyang, Liaoning, China.ORCID 0000-0001-5911-9127
Hang XueDepartment of Anesthesiology, Shengjing Hospital of China Medical University, Shenyang, Liaoning, China.
Qiushi GaoDepartment of Anesthesiology, Shengjing Hospital of China Medical University, Shenyang, Liaoning, China.
Yahan ZhangDepartment of Anesthesiology, Shengjing Hospital of China Medical University, Shenyang, Liaoning, China.
Changming WangDepartment of Anesthesiology, People's Hospital of China Medical University (Liaoning Provincial People's Hospital), Shenyang, Liaoning, China.
Ping ZhaoDepartment of Anesthesiology, Shengjing Hospital of China Medical University, Shenyang, Liaoning, China.ORCID 0000-0001-6392-5391
China Medical University · CNLiaoning Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsHypoxic-ischemic brain injury (HIBI) often results in cognitive impairments. Herein, we investigated the roles of ferroptosis in HIBI and the underlying signaling pathways.

methodsFerrostatin-1 (Fer-1) or resveratrol (Res) treatments were administered intracerebroventricularly 30 min before HIBI in 7-day-old rats. Glutathione peroxidase 4 (GPx4) expression, malondialdehyde (MDA) concentration, iron content, mitochondrial morphology, and the expression of silent information regulator factor 2-related enzyme 1 (SIRT1) and nuclear factor erythroid-2-related factor 2 (Nrf2) were measured after HIBI. Additionally, the weight ratio of left/right hemisphere, brain morphology, Nissl staining, and the Morris water maze test were conducted to estimate brain damage.

resultsAt 24-h post-HIBI, GPx4 expression was decreased, and MDA concentration and iron content were increased in the hippocampus. HIBI led to mitochondrial atrophy, brain atrophy/damage, and resultant learning and memory impairments, which were alleviated by Fer-1-mediated inhibition of ferroptosis. Furthermore, Res-mediated SIRT1 upregulation increased Nrf2 and GPx4 expression, thereby attenuating ferroptosis, reducing brain atrophy/damage, and improving learning and memory abilities.

conclusionThe results demonstrated that during HIBI, ferroptosis occurs via the SIRT1/Nrf2/GPx4 signaling pathway, suggesting it as a potential therapeutic target for inhibiting ferroptosis and ameliorating HIBI-induced cognitive impairments.

Indexed as

Brain InjuriesFerroptosisHypoxia-Ischemia, BrainAnimalsAnimals, NewbornAtrophyCyclohexylaminesIronNF-E2-Related Factor 2PhenylenediaminesRatsSignal TransductionSirtuin 1Cyclohexylaminesferrostatin-1IronNF-E2-Related Factor 2PhenylenediaminesSirt1 protein, ratSirtuin 1ferroptosisglutathione peroxidase 4hypoxic-ischemic brain injurylearning and memory impairmentsresveratrol

Identifiers

PMID36184790
PMCPMC9627393
OpenAlexW4300689649

What OpenQuestion holds

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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.