Evidence map›Paper›PMID 29239329›Full record

ArticleNeural regeneration research2017

Activation of the Akt/mTOR signaling pathway: A potential response to long-term neuronal loss in the hippocampus after sepsis.

Jia-Nan Guo, Lin-Yu Tian, Wen-Yu Liu, Jie Mu, Dong Zhou

Open access · goldAbstract read
In one paragraph

Article in Neural regeneration research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 21% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.

  1. Pooled it
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  4. Article
  5. Review
  6. mTOR inhibition impairs extinction memory reconsolidation.Learning & memory (Cold Spring Harbor, N.Y.) · 2021
    Article
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  8. 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

5 authors at 2 institutions in 1 country.

Jia-Nan GuoDepartment of Neurology, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China.
Lin-Yu TianDepartment of Neurology, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China.
Wen-Yu LiuDepartment of Neurology, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China.
Jie MuDepartment of Neurology, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China.
Dong ZhouDepartment of Neurology, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China.
Sichuan University · CNWest China Hospital of Sichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Survivors of sepsis may suffer chronic cognitive impairment as a long-term sequela. However, the precise mechanisms of cognitive dysfunction after sepsis are not well understood. We employed the cecal ligation-and-puncture-induced septic mouse model. We observed elevated phosphorylation of Akt, mammalian target of rapamycin (mTOR) and p70S6K on days 14 and 60, progressive neuronal loss in the cornu ammonis 1 region, and abnormal neuronal morphology in the hippocampus in the sepsis mouse model. These findings indicate that changes in neuronal morphology and number in the hippocampus after sepsis were associated with strong activation of the Akt/mTOR signaling pathway, and may reflect a "self-rescuing" feedback response to neuronal loss after sepsis.

Indexed as

Aktcognitive impairmenthippocampusmTORnerve regenerationneural hypertrophyneural regenerationneuronsp70S6Kphosphorylationsepsis

Identifiers

PMID29239329
PMCPMC5745837
OpenAlexW2770407267

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.