Evidence map›Paper›PMID 28886009›Full record

ArticleMolecular psychiatry2017

Tau-mediated iron export prevents ferroptotic damage after ischemic stroke.

Q-Z Tuo, P Lei, K A Jackman, X-L Li, H Xiong, X-L Li, Z-Y Liuyang, L Roisman, S-T Zhang, S Ayton and 11 more

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Molecular psychiatry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 412 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
412citing papers in PubMed, 1 pooled it
14.4field-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

412 citing papers in PubMed, 1 synthesis or guideline pooled it, 706 citations in OpenAlex.

  1. Pooled it
  2. Ferroptosis in health and disease.Molecular biomedicine · 2026
    Review
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  4. Circular RNAs in ferroptosis regulation and tumor progression of gynecological and breast cancers: molecular mechanisms and therapeutic potential.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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352 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

21 authors at 5 institutions in 2 countries.

Q-Z TuoDepartment of Pathophysiology, Key Laboratory of Ministry of Education for Neurological Disorders, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
P LeiOxidation Biology Unit, Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Melbourne, VIC, Australia.
K A JackmanOxidation Biology Unit, Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Melbourne, VIC, Australia.
X-L LiDepartment of Neurology and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, and Collaborative Innovation Center for Biotherapy, Sichuan, China.
H XiongDepartment of Neurology and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, and Collaborative Innovation Center for Biotherapy, Sichuan, China.
X-L LiOxidation Biology Unit, Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Melbourne, VIC, Australia.
Z-Y LiuyangDepartment of Pathophysiology, Key Laboratory of Ministry of Education for Neurological Disorders, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
L RoismanDepartment of Pathology, The University of Melbourne, Melbourne, VIC, Australia.
S-T ZhangDepartment of Neurology and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, and Collaborative Innovation Center for Biotherapy, Sichuan, China.
S AytonOxidation Biology Unit, Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Melbourne, VIC, Australia.
Q WangDepartment of Neurology and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, and Collaborative Innovation Center for Biotherapy, Sichuan, China.
P J CrouchDepartment of Pathology, The University of Melbourne, Melbourne, VIC, Australia.
K GanioOxidation Biology Unit, Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Melbourne, VIC, Australia.
X-C WangDepartment of Pathophysiology, Key Laboratory of Ministry of Education for Neurological Disorders, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
L PeiDepartment of Neurobiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Hubei, China.
P A AdlardOxidation Biology Unit, Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Melbourne, VIC, Australia.
Y-M LuDepartment of Pathophysiology, Key Laboratory of Ministry of Education for Neurological Disorders, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
R CappaiDepartment of Pathology, The University of Melbourne, Melbourne, VIC, Australia.
J-Z WangDepartment of Pathophysiology, Key Laboratory of Ministry of Education for Neurological Disorders, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
R LiuDepartment of Pathophysiology, Key Laboratory of Ministry of Education for Neurological Disorders, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
A I BushOxidation Biology Unit, Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Melbourne, VIC, Australia.
Huazhong University of Science and Technology · CNUniversity of Melbourne · AUFlorey Institute of Neuroscience and Mental Health · AUSichuan University · CNHarbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Functional failure of tau contributes to age-dependent, iron-mediated neurotoxicity, and as iron accumulates in ischemic stroke tissue, we hypothesized that tau failure may exaggerate ischemia-reperfusion-related toxicity. Indeed, unilateral, transient middle cerebral artery occlusion (MCAO) suppressed hemispheric tau and increased iron levels in young (3-month-old) mice and rats. Wild-type mice were protected by iron-targeted interventions: ceruloplasmin and amyloid precursor protein ectodomain, as well as ferroptosis inhibitors. At this age, tau-knockout mice did not express elevated brain iron and were protected against hemispheric reperfusion injury following MCAO, indicating that tau suppression may prevent ferroptosis. However, the accelerated age-dependent brain iron accumulation that occurs in tau-knockout mice at 12 months of age negated the protective benefit of tau suppression against MCAO-induced focal cerebral ischemia-reperfusion injury. The protective benefit of tau knockout was revived in older mice by iron-targeting interventions. These findings introduce tau-iron interaction as a pleiotropic modulator of ferroptosis and ischemic stroke outcome.

Indexed as

Age FactorsAnimalsBrainBrain InjuriesBrain IschemiaDisease Models, AnimalInfarction, Middle Cerebral ArteryIronMaleMiceMice, KnockoutNeuronsRatsRats, Sprague-DawleyReperfusion InjuryStrokeIronMapt protein, mousetau Proteins

Identifiers

PMID28886009
OpenAlexW2752949400

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.