Evidence map›Paper›PMID 27614618›Full record

ArticleTranslational stroke research2016

Dimethyl Fumarate and Monomethyl Fumarate Promote Post-Ischemic Recovery in Mice.

Yang Yao, Weimin Miao, Zhijia Liu, Wei Han, Kaibin Shi, Yi Shen, Handong Li, Qiang Liu, Ying Fu, DeRen Huang and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Translational stroke research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
6.0field-weighted citation impact, top 4% 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

61 citing papers in PubMed, 104 citations in OpenAlex.

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1 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

11 authors at 4 institutions in 2 countries.

Yang YaoDepartment of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Weimin MiaoThe State Key Laboratory of Experimental Hematology, Chinese Academy of Medical Sciences and Peking Union Medical College, 288 Nanjing Road, Tianjin, 300020, China.
Zhijia LiuDepartment of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Wei HanDepartment of Radiology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Kaibin ShiDepartment of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Yi ShenDepartment of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Handong LiDepartment of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Qiang LiuDepartment of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Ying FuDepartment of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, 300052, China.
DeRen HuangNeurology and Neuroscience Associates, Unity Health Network, Akron, OH, USA.
Fu-Dong ShiDepartment of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, 300052, China. fshi@tmu.edu.cn.
Tianjin Medical University General Hospital · CNBarrow Neurological Institute · USChinese Academy of Medical Sciences & Peking Union Medical College · CNHealth Net · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress plays an important role in cerebral ischemia-reperfusion injury. Dimethyl fumarate (DMF) and its primary metabolite monomethyl fumarate (MMF) are antioxidant agents that can activate the nuclear factor erythroid-2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway and induce the expression of antioxidant proteins. Here, we evaluated the impact of DMF and MMF on ischemia-induced brain injury and whether the Nrf2 pathway mediates the effects provided by DMF and MMF in cerebral ischemia-reperfusion injury. Using a mouse model of transient focal brain ischemia, we show that DMF and MMF significantly reduce neurological deficits, infarct volume, brain edema, and cell death. Further, DMF and MMF suppress glial activation following brain ischemia. Importantly, the protection of DMF and MMF was mostly evident during the subacute stage and was abolished in Nrf2

Indexed as

AnimalsBrain EdemaCalcium-Binding ProteinsDimethyl FumarateDisease Models, AnimalDose-Response Relationship, DrugFumaratesGlial Fibrillary Acidic ProteinGlutathioneImmunosuppressive AgentsInfarction, Middle Cerebral ArteryMaleatesMalondialdehydeMiceMice, Inbred C57BLMicrofilament ProteinsAif1 protein, mouseCalcium-Binding Proteinscitraconic acidDimethyl FumarateFumaratesGlial Fibrillary Acidic ProteinGlutathioneImmunosuppressive AgentsMaleatesMalondialdehydeMicrofilament ProteinsNeuroprotective AgentsNfe2l2 protein, mouseNF-E2-Related Factor 2Dimethyl fumarateHO-1Monomethyl fumarateNrf2Stroke

Identifiers

PMID27614618
PMCPMC5065588
OpenAlexW2518578718

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.