Evidence map›Paper›PMID 39138706›Full record

ArticleNeuromolecular medicine2024

Activation of GPR30 Ameliorates Cerebral Ischemia-Reperfusion Injury by Suppressing Ferroptosis Through Nrf2/GPX4 Signaling Pathway.

Yong-Qiang Zhang, Ting Sun, Zhen Zhao, Jing Fu, Le Yang, Yuan Xu, Jing-Feng Zhao, Xiu-Ling Tang, An Liu, Ming-Gao Zhao

Abstract read
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In one paragraph

Article in Neuromolecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

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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

10 authors.

Yong-Qiang Zhang *Precision Pharmacy & Drug Development Center, Department of Pharmacy, Tangdu Hospital, Air Force Medical University, Xi'an, Shaanxi, China.
Ting Sun *Precision Pharmacy & Drug Development Center, Department of Pharmacy, Tangdu Hospital, Air Force Medical University, Xi'an, Shaanxi, China.
Zhen Zhao *Precision Pharmacy & Drug Development Center, Department of Pharmacy, Tangdu Hospital, Air Force Medical University, Xi'an, Shaanxi, China.
Jing FuPrecision Pharmacy & Drug Development Center, Department of Pharmacy, Tangdu Hospital, Air Force Medical University, Xi'an, Shaanxi, China.
Le YangPrecision Pharmacy & Drug Development Center, Department of Pharmacy, Tangdu Hospital, Air Force Medical University, Xi'an, Shaanxi, China.
Yuan XuPrecision Pharmacy & Drug Development Center, Department of Pharmacy, Tangdu Hospital, Air Force Medical University, Xi'an, Shaanxi, China.
Jing-Feng ZhaoDepartment of Chemistry, School of Pharmacy, Air Force Medical University, Xi'an, Shaanxi, China.
Xiu-Ling TangPrecision Pharmacy & Drug Development Center, Department of Pharmacy, Tangdu Hospital, Air Force Medical University, Xi'an, Shaanxi, China.
An LiuPrecision Pharmacy & Drug Development Center, Department of Pharmacy, Tangdu Hospital, Air Force Medical University, Xi'an, Shaanxi, China. anran1222@163.com.
Ming-Gao ZhaoPrecision Pharmacy & Drug Development Center, Department of Pharmacy, Tangdu Hospital, Air Force Medical University, Xi'an, Shaanxi, China. minggao@fmmu.edu.cn.

Funding

Key Research and Development Program in Shaanxi Province of China fund no.2022SF-314This work was supported by the National Natural Science Foundation of China No. 82104158
6 · The paper itself

Abstract

The newly identified estrogen receptor, G protein-coupled receptor 30 (GPR30), is prevalent in the brain and has been shown to provide significant neuroprotection. Recent studies have linked ferroptosis, a newly characterized form of programmed cell death, closely with cerebral ischemia-reperfusion injury (CIRI), highlighting it as a major contributing factor. Consequently, our research aimed to explore the potential of GPR30 targeting in controlling neuronal ferroptosis and lessening CIRI impacts. Results indicated that GPR30 activation not only improved neurological outcomes and decreased infarct size in a mouse model but also lessened iron accumulation and malondialdehyde formation post-middle cerebral artery occlusion (MCAO). This protective effect extended to increased levels of Nrf2 and GPX4 proteins. Similar protective results were replicated in PC12 cells subjected to Oxygen Glucose Deprivation and Reoxygenation (OGD/R) using the GPR30-specific agonist G1. Importantly, inhibition of Nrf2 with ML385 curtailed the neuroprotective effects of GPR30 activation, suggesting that GPR30 mitigates CIRI primarily through inhibition of neuronal ferroptosis via upregulation of Nrf2 and GPX4.

Indexed as

FerroptosisInfarction, Middle Cerebral ArteryMice, Inbred C57BLNF-E2-Related Factor 2Phospholipid Hydroperoxide Glutathione PeroxidaseReceptors, EstrogenReceptors, G-Protein-CoupledReperfusion InjurySignal TransductionAnimalsDisease Models, AnimalMaleMiceNeuroprotective AgentsPC12 CellsRatsglutathione peroxidase 4, mouseglutathione peroxidase 4, ratGPER1 protein, mouseGper1 protein, ratNeuroprotective AgentsNfe2l2 protein, mouseNfe2l2 protein, ratNF-E2-Related Factor 2Phospholipid Hydroperoxide Glutathione PeroxidaseReceptors, EstrogenReceptors, G-Protein-CoupledCerebral ischemia–reperfusion injuryFerroptosisGlutathione peroxidase 4GPR30Nuclear factor erythroid-2-related factor 2

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Registered trials

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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.