Evidence map›Paper›PMID 36631632›Full record

ArticleTranslational stroke research2024

Netrin-1 Alleviates Early Brain Injury by Regulating Ferroptosis via the PPARγ/Nrf2/GPX4 Signaling Pathway Following Subarachnoid Hemorrhage.

Junhui Chen, Yuhai Wang, Mingchang Li, Xun Zhu, Zhuanghua Liu, Qianxue Chen, Kun Xiong

Abstract read
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In one paragraph

Article in Translational stroke research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
17.6field-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

46 citing papers in PubMed, 68 citations in OpenAlex.

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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

7 authors at 4 institutions in 1 country.

Junhui Chen *Department of Human Anatomy and Neurobiology, School of Basic Medical Science, Central South University, Changsha, Hunan Province, China.
Yuhai Wang *Department of Neurosurgery, 904th Hospital of Joint Logistic Support Force of PLA, Wuxi Clinical College of Anhui Medical University, Wuxi, 214044, China.
Mingchang Li *Department of Neurosurgery, Renmin Hospital of Wuhan University, No. 9 Zhangzhidong Road, Wuchang District, Wuhan, 430072, Hubei Province, China.
Xun ZhuDepartment of Neurosurgery, The Second Hospital of Tianjin Medical University, Tianjin, China.
Zhuanghua LiuDepartment of Neurosurgery, 904th Hospital of Joint Logistic Support Force of PLA, Wuxi Clinical College of Anhui Medical University, Wuxi, 214044, China.
Qianxue ChenDepartment of Neurosurgery, Renmin Hospital of Wuhan University, No. 9 Zhangzhidong Road, Wuchang District, Wuhan, 430072, Hubei Province, China. cqxwhu@126.com.
Kun XiongDepartment of Human Anatomy and Neurobiology, School of Basic Medical Science, Central South University, Changsha, Hunan Province, China. xiongkun2001@163.com.
Wuhan University · CNAnhui Medical University · CNCentral South University · CNTianjin Medical University · CN

Funding

National Natural Science Foundation of China 81871589Natural Science Foundation of Jiangsu Province BK20201140Top Talent Support Program for young and middle-aged people of Wuxi Health Committee HB2020119Wuxi science and technology development foundation N20201008
6 · The paper itself

Abstract

Subarachnoid hemorrhage (SAH) is a type of stroke with high morbidity and mortality. Netrin-1 (NTN-1) can alleviate early brain injury (EBI) following SAH by enhancing peroxisome proliferator-activated receptor gamma (PPARγ), which is an important transcriptional factor modulating lipid metabolism. Ferroptosis is a newly discovered type of cell death related to lipid metabolism. However, the specific function of ferroptosis in NTN-1-mediated neuroprotection following SAH is still unclear. This study aimed to evaluate the neuroprotective effects and the possible molecular basis of NTN-1 in SAH-induced EBI by modulating neuronal ferroptosis using the filament perforations model of SAH in mice and the hemin-stimulated neuron injury model in HT22 cells. NTN-1 or a vehicle was administered 2 h following SAH. We examined neuronal death, brain water content, neurological score, and mortality. NTN-1 treatment led to elevated survival probability, greater survival of neurons, and increased neurological score, indicating that NTN-1-inhibited ferroptosis ameliorated neuron death in vivo/in vitro in response to SAH. Furthermore, NTN-1 treatment enhanced the expression of PPARγ, nuclear factor erythroid 2-related factor 2 (Nrf2), and glutathione peroxidase 4 (GPX4), which are essential regulators of ferroptosis in EBI after SAH. The findings show that NTN-1 improves neurological outcomes in mice and protects neurons from death caused by neuronal ferroptosis. Furthermore, the mechanism underlying NTN-1 neuroprotection is correlated with the inhibition of ferroptosis, attenuating cell death via the PPARγ/Nrf2/GPX4 pathway and coenzyme Q10-ferroptosis suppressor protein 1 (CoQ10-FSP1) pathway.

Indexed as

Brain InjuriesFerroptosisSubarachnoid HemorrhageAnimalsMiceNetrin-1NF-E2-Related Factor 2PPAR gammaRatsRats, Sprague-DawleySignal TransductionNetrin-1NF-E2-Related Factor 2PPAR gammaEarly brain injuryFerroptosisGlutathione peroxidase 4 (GPX4)Netrin-1Nuclear factor erythroid 2-related factor 2 (Nrf2)Subarachnoid hemorrhage (SAH)

Identifiers

PMID36631632
OpenAlexW4315618950

What OpenQuestion holds

Textmetadata
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.