Evidence map›Paper›PMID 39397243›Full record

ReviewZoological research2024

Ferroptosis in ischemic stroke: Animal models and mechanisms.

Qing-Zhang Tuo, Peng Lei

Abstract readReview
In one paragraph

Review in Zoological research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing 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

27 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

2 authors.

Qing-Zhang TuoDepartment of Geriatrics and State Key Laboratory of Biotherapy, National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, China. E-mail: qing-zhang.tuo@scu.edu.cn.
Peng LeiDepartment of Neurology and State Key Laboratory of Biotherapy, National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, China. E-mail: peng.lei@scu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Stroke is a major cause of death and disability worldwide, with the majority of cases resulting from ischemic events due to arterial occlusion. Current therapeutic approaches focus on rapid reperfusion through intravenous thrombolysis and intravascular thrombectomy. Although these interventions can mitigate long-term disability, reperfusion itself may induce neuronal injury. The exact mechanisms underlying neuronal damage following cerebral ischemia have yet to be reported. Recent research suggests that ferroptosis may play a significant role in post-ischemic neuronal death, which can be targeted to prevent neuronal loss. This review explores the three essential hallmarks of ferroptosis: the presence of redox-active iron, the peroxidation of polyunsaturated fatty acid-containing phospholipids, and the loss of lipid peroxide repair capacity. The involvement of ferroptosis in neuronal injury following ischemic stroke is also explored, along with an overview of ferroptosis-associated changes in different ischemic stroke animal models. Furthermore, recent therapeutic interventions targeting the ferroptosis pathway, as well as the opportunities, difficulties, and future directions of ferroptosis-targeted therapies in ischemic stroke, are discussed.

Indexed as

Disease Models, AnimalFerroptosisIschemic StrokeAnimalsBrain IschemiaHumansStrokeAnimal modelsFerroptosisIron depositionIschemic strokeLipid peroxidation

Identifiers

PMID39397243
PMCPMC11668946

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.