Evidence map›Paper›PMID 37017405›Full record

ArticleCNS neuroscience & therapeutics2023

14, 15-EET alleviates neurological impairment through maintaining mitochondrial dynamics equilibrium via AMPK/SIRT1/FoxO1 signal pathways in mice with cerebral ischemia reperfusion.

Jing Tang, Yiang Chen, Jinyuan Li, Shuo Yan, Zenan Wang, Xinyu Deng, Ke Feng, Yanshuo Zhang, Chunrong Chen, Huixia Geng and 2 more

Open access · goldAbstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

12 citing papers in PubMed, 32 citations in OpenAlex.

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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

12 authors at 1 institution in 1 country.

Jing TangThe School of Life Sciences, Henan University, 475000, Henan Province, Kaifeng, P. R. China.
Yiang ChenThe School of Life Sciences, Henan University, 475000, Henan Province, Kaifeng, P. R. China.
Jinyuan LiThe School of Life Sciences, Henan University, 475000, Henan Province, Kaifeng, P. R. China.
Shuo YanThe School of Life Sciences, Henan University, 475000, Henan Province, Kaifeng, P. R. China.
Zenan WangThe School of Life Sciences, Henan University, 475000, Henan Province, Kaifeng, P. R. China.
Xinyu DengThe School of Life Sciences, Henan University, 475000, Henan Province, Kaifeng, P. R. China.
Ke FengThe School of Life Sciences, Henan University, 475000, Henan Province, Kaifeng, P. R. China.
Yanshuo ZhangThe School of Life Sciences, Henan University, 475000, Henan Province, Kaifeng, P. R. China.
Chunrong ChenThe School of Life Sciences, Henan University, 475000, Henan Province, Kaifeng, P. R. China.
Huixia GengThe School of Life Sciences, Henan University, 475000, Henan Province, Kaifeng, P. R. China.
Yanming WangThe School of Life Sciences, Henan University, 475000, Henan Province, Kaifeng, P. R. China.
Lai WangThe School of Life Sciences, Henan University, 475000, Henan Province, Kaifeng, P. R. China.ORCID 0000-0002-3323-7210
Henan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimTo explore whether 14, 15-EET regulates mitochondrial dynamics to exert neuroprotective effects after cerebral ischemia-reperfusion and its underlying mechanisms.

methodsThe mouse middle cerebral artery occlusion reperfusion model was used to observe brain infarct volume and neuronal apoptosis by TTC staining and Tunel assay, modified neurological severity score to detect neurological impairment, HE staining and Nissl staining to observe neuron damage, western blot and immunofluorescence methods to detect the expression of mitochondrial dynamics-related proteins, transmission electron microscopy, and Golgi-Cox staining to detect mitochondrial morphology and neuronal dendritic spines.

results14, 15-EET reduced the neuronal apoptosis and cerebral infarction volume induced by middle cerebral artery occlusion reperfusion (MCAO/R), inhibited the degradation of dendritic spines, maintained the structural integrity of neurons, and alleviated neurological impairment. Cerebral ischemia-reperfusion induces mitochondrial dynamics disorders, upregulates the expression of the mitochondrial division protein Fis 1, and inhibits the expression of mitochondrial fusion proteins MFN1, MFN2, and OPA1, while 14, 15-EET treatment reverses this process. Mechanistic studies have shown that 14, 15-EET promotes the phosphorylation of AMPK, upregulates the expression of SIRT1 and phosphorylation of FoxO1, thereby inhibiting mitochondrial division and promoting mitochondrial fusion, preserving mitochondrial dynamics, maintaining neuronal morphological and structural integrity, and alleviating neurological impairment induced by middle cerebral artery occlusion reperfusion. Compound C treatment diminishes the neuroprotective effect of 14, 15-EET following MCAO/R in mice.

conclusionThis study elucidates the novel neuroprotective mechanism of 14, 15-EET, providing a novel approach for the development of drugs based on mitochondrial dynamics.

Indexed as

Brain IschemiaNeuroprotective AgentsReperfusion InjuryAMP-Activated Protein KinasesAnimalsApoptosisInfarction, Middle Cerebral ArteryMiceMitochondrial DynamicsReperfusionSignal TransductionSirtuin 1AMP-Activated Protein KinasesNeuroprotective AgentsSirtuin 114, 15-EETcerebral ischemia reperfusionmitochondrial dynamicsneuronal apoptosis

Identifiers

PMID37017405
PMCPMC10401172
OpenAlexW4362602351

What Socratic holds

Textmetadata
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 Socratic graph.