Evidence map›Paper›PMID 33953171›Full record

ArticleCell death & disease2021

Mitochondrial ferritin attenuates cerebral ischaemia/reperfusion injury by inhibiting ferroptosis.

Peina Wang, Yanmei Cui, Qianqian Ren, Bingqi Yan, Yashuo Zhao, Peng Yu, Guofen Gao, Honglian Shi, Shiyang Chang, Yan-Zhong Chang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 131 papers.

0numbers the graph read from it
0cells of the map it votes in
131citing papers in PubMed
18.6field-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

131 citing papers in PubMed, 196 citations in OpenAlex.

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71 more citing papers are in PubMed but not listed here.

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

10 authors at 4 institutions in 2 countries.

Peina WangLaboratory of Molecular Iron Metabolism, Key Laboratory of Animal Physiology, Biochemistry and Molecular Biology of Hebei Province, Ministry of Education Key Laboratory of Molecular and Cellular Biology, College of Life Science, Hebei Normal University, 050024, Shijiazhuang, Hebei Province, China.
Yanmei CuiLaboratory of Molecular Iron Metabolism, Key Laboratory of Animal Physiology, Biochemistry and Molecular Biology of Hebei Province, Ministry of Education Key Laboratory of Molecular and Cellular Biology, College of Life Science, Hebei Normal University, 050024, Shijiazhuang, Hebei Province, China.
Qianqian RenLaboratory of Molecular Iron Metabolism, Key Laboratory of Animal Physiology, Biochemistry and Molecular Biology of Hebei Province, Ministry of Education Key Laboratory of Molecular and Cellular Biology, College of Life Science, Hebei Normal University, 050024, Shijiazhuang, Hebei Province, China.
Bingqi YanLaboratory of Molecular Iron Metabolism, Key Laboratory of Animal Physiology, Biochemistry and Molecular Biology of Hebei Province, Ministry of Education Key Laboratory of Molecular and Cellular Biology, College of Life Science, Hebei Normal University, 050024, Shijiazhuang, Hebei Province, China.
Yashuo ZhaoLaboratory of Molecular Iron Metabolism, Key Laboratory of Animal Physiology, Biochemistry and Molecular Biology of Hebei Province, Ministry of Education Key Laboratory of Molecular and Cellular Biology, College of Life Science, Hebei Normal University, 050024, Shijiazhuang, Hebei Province, China.
Peng YuLaboratory of Molecular Iron Metabolism, Key Laboratory of Animal Physiology, Biochemistry and Molecular Biology of Hebei Province, Ministry of Education Key Laboratory of Molecular and Cellular Biology, College of Life Science, Hebei Normal University, 050024, Shijiazhuang, Hebei Province, China.
Guofen GaoLaboratory of Molecular Iron Metabolism, Key Laboratory of Animal Physiology, Biochemistry and Molecular Biology of Hebei Province, Ministry of Education Key Laboratory of Molecular and Cellular Biology, College of Life Science, Hebei Normal University, 050024, Shijiazhuang, Hebei Province, China.
Honglian ShiDepartment of Pharmacology and Toxicology, School of Pharmacy, University of Kansas, 1251 Wescoe Hall Drive, Malott Hall 5044, Lawrence, KS, 66045, USA.
Shiyang ChangCollege of basic medicine, Hebei Medical University, 050017, Shijiazhuang, Hebei Province, China. changshiyangie@163.com.
Yan-Zhong ChangLaboratory of Molecular Iron Metabolism, Key Laboratory of Animal Physiology, Biochemistry and Molecular Biology of Hebei Province, Ministry of Education Key Laboratory of Molecular and Cellular Biology, College of Life Science, Hebei Normal University, 050024, Shijiazhuang, Hebei Province, China. frankyzchang@yahoo.com.hk.ORCID http://orcid.org/0000-0002-6386-9649
Hebei Normal University · CNHebei Medical University · CNHebei University of Chinese Medicine · CNUniversity of Kansas · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ischaemic stroke is becoming the most common cerebral disease in aging populations, but the underlying molecular mechanism of the disease has not yet been fully elucidated. Increasing evidence has indicated that an excess of iron contributes to brain damage in cerebral ischaemia/reperfusion (I/R) injury. Although mitochondrial ferritin (FtMt) plays a critical role in iron homeostasis, the molecular function of FtMt in I/R remains unknown. We herein report that FtMt levels are upregulated in the ischaemic brains of mice. Mice lacking FtMt experience more severe brain damage and neurological deficits, accompanied by typical molecular features of ferroptosis, including increased lipid peroxidation and disturbed glutathione (GSH) after cerebral I/R. Conversely, FtMt overexpression reverses these changes. Further investigation shows that Ftmt ablation promotes I/R-induced inflammation and hepcidin-mediated decreases in ferroportin1, thus markedly increasing total and chelatable iron. The elevated iron consequently facilitates ferroptosis in the brain of I/R. In brief, our results provide evidence that FtMt plays a critical role in protecting against cerebral I/R-induced ferroptosis and subsequent brain damage, thus providing a new potential target for the treatment/prevention of ischaemic stroke.

Indexed as

AnimalsCell DeathFerritinsFerroptosisHumansMiceMice, KnockoutMitochondriaReperfusion InjuryFerritins

Identifiers

PMID33953171
PMCPMC8099895
OpenAlexW3159261210

What OpenQuestion holds

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LicenceCC BY
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.