Evidence map›Paper›PMID 37676391›Full record

ArticleMolecular neurobiology2024

Deferoxamine Mitigates Ferroptosis and Inflammation in Hippocampal Neurons After Subarachnoid Hemorrhage by Activating the Nrf2/TXNRD1 Axis.

Junting Hu, Meixiong Cheng, Chonggui Jiang, Ling Liu, Zongze He, Lingtong Liu, Yuanpeng Yao, Zhili Li, Qi Wang

Abstract read
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In one paragraph

Article in Molecular neurobiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
6.2field-weighted citation impact, top 3% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.

  1. Pooled it
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  15. Ferroptosis in organ fibrosis: From mechanisms to therapeutic medicines.Journal of translational internal medicine · 2024
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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

9 authors at 1 institution in 1 country.

Junting HuDepartment of Neurosurgery, School of Medicine, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, No. 32, Section 2, West 1St Ring Road, Chengdu, 610072, Sichuan, China.
Meixiong ChengDepartment of Neurosurgery, School of Medicine, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, No. 32, Section 2, West 1St Ring Road, Chengdu, 610072, Sichuan, China.
Chonggui JiangDepartment of Neurosurgery, School of Medicine, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, No. 32, Section 2, West 1St Ring Road, Chengdu, 610072, Sichuan, China.
Ling LiuDepartment of Neurosurgery, School of Medicine, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, No. 32, Section 2, West 1St Ring Road, Chengdu, 610072, Sichuan, China.
Zongze HeDepartment of Neurosurgery, School of Medicine, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, No. 32, Section 2, West 1St Ring Road, Chengdu, 610072, Sichuan, China.
Lingtong LiuDepartment of Neurosurgery, School of Medicine, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, No. 32, Section 2, West 1St Ring Road, Chengdu, 610072, Sichuan, China.
Yuanpeng YaoDepartment of Neurosurgery, School of Medicine, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, No. 32, Section 2, West 1St Ring Road, Chengdu, 610072, Sichuan, China.
Zhili LiDepartment of Neurosurgery, School of Medicine, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, No. 32, Section 2, West 1St Ring Road, Chengdu, 610072, Sichuan, China. 2862826488@qq.com.
Qi WangDepartment of Neurosurgery, School of Medicine, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, No. 32, Section 2, West 1St Ring Road, Chengdu, 610072, Sichuan, China. Qiwang_2013@163.com.ORCID http://orcid.org/0009-0002-6956-486X
University of Electronic Science and Technology of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ferroptosis is a distinct peroxidation-driven form of cell death tightly involved in subarachnoid hemorrhage (SAH). This study delved into the mechanism of deferoxamine (DFO, an iron chelator) in SAH-induced ferroptosis and inflammation. SAH mouse models were established by endovascular perforation method and injected intraperitoneally with DFO, or intraventricularly injected with the Nrf2 pathway inhibitor ML385 before SAH, followed by detection of neurological function, blood-brain barrier (BBB) permeability, and brain water content. Apoptotic level of hippocampal neurons, symbolic changes of ferroptosis, and levels of pro-inflammatory cytokines were assessed using TUNEL staining, Western blotting, colorimetry, and ELISA. The localization and expression of nuclear factor-erythroid 2-related factor 2 (Nrf2) were detected. HT22 cells were exposed to Hemin as in vitro SAH models and treated with FIN56 to induce ferroptosis, followed by evaluation of the effects of DFO on FIN56-treated HT22 cells. The regulation of Nrf2 in thioredoxin reductase 1 (TXNRD1) was analyzed by co-immunoprecipitation and Western blotting. Moreover, HT22 cells were treated with DFO and ML385 to identify the role of DFO in the Nrf2/TXNRD1 axis. DFO extenuated brain injury, and ferroptosis and inflammation in hippocampal neurons of SAH mice. Nrf2 localized at the CA1 region of hippocampal neurons, and DFO stimulated nuclear translocation of Nrf2 protein in hippocampal neurons of SAH mice. Additionally, DFO inhibited ferroptosis and inflammatory responses in FIN56-induced HT22 cells. Nrf2 positively regulated TXNRD1 protein expression. Indeed, DFO alleviated FIN56-induced ferroptosis and inflammation via activation of the Nrf2/TXNRD1 axis. DFO alleviated neurological deficits, BBB disruption, brain edema, and brain injury in mice after SAH by inhibiting hippocampal neuron ferroptosis via the Nrf2/TXNRD1 axis. DFO ameliorates SAH-induced ferroptosis and inflammatory responses in hippocampal neurons by activating the Nrf2/TXNRD1 axis.

Indexed as

Brain InjuriesFerroptosisSubarachnoid HemorrhageAnimalsDeferoxamineHippocampusInflammationMiceNeuronsNF-E2-Related Factor 2RatsRats, Sprague-DawleyThioredoxin Reductase 1DeferoxamineNF-E2-Related Factor 2Thioredoxin Reductase 1DeferoxamineFerroptosis, Inflammatory responseFIN56GPX4Hippocampal neuronHT22 cellNrf2/TXNRD1 axisSubarachnoid hemorrhage

Identifiers

PMID37676391
OpenAlexW4386507378

What OpenQuestion holds

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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.