Evidence map›Paper›PMID 29348559›Full record

ArticleScientific reports2018

PLK1 protects against sepsis-induced intestinal barrier dysfunction.

Yingya Cao, Qun Chen, Zhen Wang, Tao Yu, Jingyi Wu, Xiaogan Jiang, Xiaoju Jin, Weihua Lu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.2field-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

16 citing papers in PubMed, 30 citations in OpenAlex.

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  12. Sepsis induces variation of intestinal barrier function in different phase through nuclear factor kappa B signaling.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2021
    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

8 authors at 2 institutions in 1 country.

Yingya CaoDepartment of Intensive Care Unit, Yijishan Hospital, Wannan Medical College, Wuhu, 241001, Anhui, China.
Qun ChenDepartment of Intensive Care Unit, Yijishan Hospital, Wannan Medical College, Wuhu, 241001, Anhui, China.
Zhen WangDepartment of Intensive Care Unit, Yijishan Hospital, Wannan Medical College, Wuhu, 241001, Anhui, China.
Tao YuDepartment of Intensive Care Unit, Yijishan Hospital, Wannan Medical College, Wuhu, 241001, Anhui, China.
Jingyi WuDepartment of Intensive Care Unit, Yijishan Hospital, Wannan Medical College, Wuhu, 241001, Anhui, China.
Xiaogan JiangDepartment of Intensive Care Unit, Yijishan Hospital, Wannan Medical College, Wuhu, 241001, Anhui, China.
Xiaoju JinDepartment of Intensive Care Unit, Yijishan Hospital, Wannan Medical College, Wuhu, 241001, Anhui, China.
Weihua LuDepartment of Intensive Care Unit, Yijishan Hospital, Wannan Medical College, Wuhu, 241001, Anhui, China. lwh683@126.com.
Wannan Medical College · CNFirst Affiliated Hospital of Wannan Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sepsis and sepsis-associated intestinal barrier dysfunction are common in intensive care units, with high mortality. The aim of this study is to investigate whether Polo-like kinase 1 (PLK1) ameliorates sepsis-induced intestinal barrier dysfunction in the intestinal epithelium. The mouse intestinal barrier was disrupted after Lipopolysaccharide (LPS) injection due to intestinal epithelial cell apoptosis and proliferation inhibition, accompanied by decreased PLK1. In HT-29 intestinal epithelial cells, LPS stimulation induced cell apoptosis and inhibited cell proliferation. Overexpression of PLK1 partly rescued the apoptosis and proliferation inhibition in HT29 cells caused by LPS. Finally, LPS stimulation promoted the reduction of PLK1, resulting in apoptosis and proliferation inhibition in intestinal epithelial cells, disrupting the intestinal epithelial barrier. These findings indicate that PLK1 might be a potential therapeutic target for the treatment of sepsis-induced intestinal barrier dysfunction.

Indexed as

AnimalsApoptosisBiomarkersCell Cycle ProteinsCell LineCell Membrane PermeabilityCell ProliferationDisease Models, AnimalGene Expression RegulationHumansIntestinal DiseasesIntestinal MucosaLipopolysaccharidesMaleMicePolo-Like Kinase 1BiomarkersCell Cycle ProteinsLipopolysaccharidesPolo-Like Kinase 1Protein Serine-Threonine KinasesProto-Oncogene Proteins

Identifiers

PMID29348559
PMCPMC5773589
OpenAlexW2782626594

What OpenQuestion holds

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LicenceCC BY
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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.