Evidence map›Paper›PMID 27283322›Full record

ArticleScientific reports2016

p38 MAPK Inhibition Improves Synaptic Plasticity and Memory in Angiotensin II-dependent Hypertensive Mice.

Hai-Long Dai, Wei-Yuan Hu, Li-Hong Jiang, Le Li, Xue-Feng Gaung, Zhi-Cheng Xiao

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

18 citing papers in PubMed, 39 citations in OpenAlex.

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  12. Involvement of p38 MAPK in Synaptic Function and Dysfunction.International journal of molecular sciences · 2020
    Review
  13. Functions of p38 MAP Kinases in the Central Nervous System.Frontiers in molecular neuroscience · 2020
    Review
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  15. Article
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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

6 authors at 3 institutions in 2 countries.

Hai-Long DaiDepartment of Cardiology, Yan'an Affiliated Hospital of Kunming Medical University, Kunming, China.
Wei-Yuan HuInstitute of Molecular and Clinical Medicine, Kunming Medical University, Kunming, China.
Li-Hong JiangDepartment of Cardiothoracic Surgery, Yan'an Affiliated Hospital of Kunming Medical University, Kunming, China.
Le LiDepartment of outpatient, Ganmei Affiliated Hospital of Kunming Medical University, Kunming, China.
Xue-Feng GaungDepartment of Cardiology, Yan'an Affiliated Hospital of Kunming Medical University, Kunming, China.
Zhi-Cheng XiaoInstitute of Molecular and Clinical Medicine, Kunming Medical University, Kunming, China.
Kunming Medical University · CNMonash University · AUYan'an Hospital Affiliated To Kunming Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pathogenesis of hypertension-related cognitive impairment has not been sufficiently clarified, new molecular targets are needed. p38 MAPK pathway plays an important role in hypertensive target organ damage. Activated p38 MAPK was seen in AD brain tissue. In this study, we found that long-term potentiation (LTP) of hippocampal CA1 was decreased, the density of the dendritic spines on the CA1 pyramidal cells was reduced, the p-p38 protein expression in hippocampus was elevated, and cognitive function was impaired in angiotensin II-dependent hypertensive C57BL/6 mice. In vivo, using a p38 heterozygous knockdown mice (p38(KI/+)) model, we showed that knockdown of p38 MAPK in hippocampus leads to the improvement of cognitive function and hippocampal synaptic plasticity in angiotensin II-dependent p38(KI/+) hypertensive mice. In vitro, LTP was improved in hippocampal slices from C57BL/6 hypertensive mice by treatment with p38MAPK inhibitor SKF86002. Our data demonstrated that p38 MAPK may be a potential therapeutic target for hypertension-related cognitive dysfunction.

Indexed as

Angiotensin IIAnimalsDendritic SpinesDisease Models, AnimalHippocampusHumansHypertensionImidazolesLong-Term PotentiationMiceNeuronal Plasticityp38 Mitogen-Activated Protein KinasesPyramidal CellsSignal TransductionThiazoles6-(4-fluorophenyl)-2,3-dihydro-5-(4-pyridinyl)imidazo(2,1-b)thiazoleAngiotensin IIImidazolesp38 Mitogen-Activated Protein KinasesThiazoles

Identifiers

PMID27283322
PMCPMC4901328
OpenAlexW2417575596

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.