Evidence map›Paper›PMID 33362556›Full record

ArticleFrontiers in pharmacology2020

Neuroprotective Effects of the Anti-cancer Drug Lapatinib Against Epileptic Seizures via Suppressing Glutathione Peroxidase 4-Dependent Ferroptosis.

Ji-Ning Jia, Xi-Xi Yin, Qin Li, Qi-Wen Guan, Nan Yang, Kang-Ni Chen, Hong-Hao Zhou, Xiao-Yuan Mao

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.3field-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

26 citing papers in PubMed, 56 citations in OpenAlex.

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  10. Ethanolic and aqueous extracts ofIBRO neuroscience reports · 2024
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  15. Article
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  17. Effects of DNA, RNA, and Protein Methylation on the Regulation of Ferroptosis.International journal of biological sciences · 2023
    Review
  18. Review
  19. Review
  20. Research progress on oxidative stress regulating different types of neuronal death caused by epileptic seizures.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Ji-Ning JiaDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, China.
Xi-Xi YinDepartment of Pediatrics, Xiangya Hospital, Central South University, Changsha, China.
Qin LiDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, China.
Qi-Wen GuanDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, China.
Nan YangDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, China.
Kang-Ni ChenDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, China.
Hong-Hao ZhouDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, China.
Xiao-Yuan MaoDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, China.
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epilepsy is a complex neurological disorder characterized by recurrent and unprovoked seizures. Neuronal death process is implicated in the development of repetitive epileptic seizures. Therefore, cell death can be harnessed for ceasing seizures and epileptogenesis. Oxidative stress is regarded as a contributing factor of neuronal death activation and there is compelling evidence supporting antioxidants hold promise in abrogating seizure-related cell modality. Lapatinib, a well-known anti-cancer drug, has been traditionally reported to exert anti-tumor effect via modulating oxidative stress and a recent work illustrates the improvement of encephalomyelitis in rodent models after lapatinib treatment. However, whether lapatinib is beneficial for inhibiting neuronal death and epileptic seizure remains unknown. Here, we found that lapatinib remarkably prevented kainic acid (KA)-epileptic seizures in mice and ferroptosis, a newly defined cell death which is associated with oxidative stress, was involved in the neuroprotection of lapatinib. In the ferroptotic cell death model, lapatinib exerted neuroprotection via restoring glutathione peroxidase 4 (GPX4). Treatment with GPX4 inhibitor ras-selective lethal small molecule 3 (RSL3) abrogated its anti-ferroptotic potential. In a mouse model of KA-triggered seizure, it was also validated that lapatinib blocked GPX4-dependent ferroptosis. It is concluded that lapatinib has neuroprotective potential against epileptic seizures via suppressing GPX4-mediated ferroptosis.

Indexed as

epileptic seizuresferroptosisglutathione peroxidase 4lapatiniblipid peroxidationneuroprotection

Identifiers

PMID33362556
PMCPMC7758233
OpenAlexW3112096528

What OpenQuestion holds

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LicenceCC BY
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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.