Evidence map›Paper›PMID 35090386›Full record

ArticleMolecular medicine (Cambridge, Mass.)2022

Omega-3 fatty acids impair miR-1-3p-dependent Notch3 down-regulation and alleviate sepsis-induced intestinal injury.

You-Lian Chen, Yin-Jing Xie, Zhen-Mi Liu, Wei-Bu Chen, Ru Zhang, Hong-Xing Ye, Wei Wang, Xue-Yan Liu, Huai-Sheng Chen

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 23% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 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

9 authors at 1 institution in 1 country.

You-Lian ChenDepartment of Critical Care Medicine, Shenzhen People's Hospital, The Second Clinical Medical College of Jinan University, The First Affiliated Hospital of South University of Science and Technology, No. 1017, Dongmen North Road, Luohu District, Shenzhen, 518020, Guangdong Province, People's Republic of China.
Yin-Jing XieClinical Laboratory, Shenzhen People's Hospital, The Second Clinical Medical College of Jinan University, The First Affiliated Hospital of South University of Science and Technology, Shenzhen, 518020, People's Republic of China.
Zhen-Mi LiuDepartment of Critical Care Medicine, Shenzhen People's Hospital, The Second Clinical Medical College of Jinan University, The First Affiliated Hospital of South University of Science and Technology, No. 1017, Dongmen North Road, Luohu District, Shenzhen, 518020, Guangdong Province, People's Republic of China.
Wei-Bu ChenClinical Laboratory, Shenzhen People's Hospital, The Second Clinical Medical College of Jinan University, The First Affiliated Hospital of South University of Science and Technology, Shenzhen, 518020, People's Republic of China.
Ru ZhangDepartment of Gastroenterology, Shenzhen People's Hospital, The Second Clinical Medical College of Jinan University, The First Affiliated Hospital of South University of Science and Technology, Shenzhen, 518020, People's Republic of China.
Hong-Xing YeDepartment of Critical Care Medicine, Shenzhen People's Hospital, The Second Clinical Medical College of Jinan University, The First Affiliated Hospital of South University of Science and Technology, No. 1017, Dongmen North Road, Luohu District, Shenzhen, 518020, Guangdong Province, People's Republic of China.
Wei WangDepartment of Endocrinology and Metabolism, Shenzhen People's Hospital, The Second Clinical Medical College of Jinan University, The First Affiliated Hospital of South University of Science and Technology, Shenzhen, 518020, People's Republic of China.
Xue-Yan LiuDepartment of Critical Care Medicine, Shenzhen People's Hospital, The Second Clinical Medical College of Jinan University, The First Affiliated Hospital of South University of Science and Technology, No. 1017, Dongmen North Road, Luohu District, Shenzhen, 518020, Guangdong Province, People's Republic of China.
Huai-Sheng ChenDepartment of Critical Care Medicine, Shenzhen People's Hospital, The Second Clinical Medical College of Jinan University, The First Affiliated Hospital of South University of Science and Technology, No. 1017, Dongmen North Road, Luohu District, Shenzhen, 518020, Guangdong Province, People's Republic of China. sunshinic@hotmail.com.ORCID 0000-0002-1480-702X
Jinan University · CN

Funding

Guangdong Natural Science Foundation Project No. 2021A1515012119Shenzhen's Sanming Project: Cooperative Research and Cultivation Project of Shenzhen People's Hospital No. SYJY201701
6 · The paper itself

Abstract

backgroundSepsis is a troublesome syndrome that can cause intestinal injury and even high mortality rates. Omega-3 fatty acids (FAs) are known to protect against intestinal damage. Accordingly, the current study set out to explore if omega-3 FAs could affect sepsis-induced intestinal injury with the involvement of the microRNA (miR)-1-3p/Notch3-Smad axis.

methodsFirst, cecal ligation and perforation (CLP) was performed to establish septic mouse models in C57BL/6J mice, and mouse intestinal epithelial MODE-K cells were induced by lipopolysaccharide (LPS) to establish sepsis cell models. The CLP-induced septic mice or LPS-exposed cells were subjected to treatment with Omega-3 FAs and activin (Smad signaling activator), miR-1-3p inhibitor and over-expressed/short hairpin RNA (oe-/sh)-Notch3 to explore their roles in inflammation, intestinal oxidative stress and cell apoptosis. A dual-luciferase reporter gene assay was further performed to verify the regulatory relationship between miR-1-3p and Notch3.

resultsOmega-3 FAs inhibited CLP-induced intestinal injury and ameliorated LPS-induced intestinal epithelial cell injury by down-regulating miR-1-3p, as evidenced by decreased levels of tumor necrosis factor-α, interleukin-1β (IL-1β) and IL-6, in addition to diminished levels of reactive oxygen species, malondialdehyde levels and superoxide dismutase activity. Furthermore, miR-1-3p could down-regulate Notch3, which inactivated the Smad pathway.

conclusionCollectively, our findings indicated that omega-3 FAs elevate the expression of Notch3 by down-regulating miR-1-3p, and then blocking the Smad pathway to alleviate intestinal epithelial inflammation and oxidative stress injury caused by sepsis.

Indexed as

Gene Expression RegulationAnimalsBiomarkersDisease ManagementDisease Models, AnimalDisease SusceptibilityFatty Acids, Omega-3Gene Expression ProfilingIntestinal DiseasesIntestinal MucosaMiceMicroRNAsModels, BiologicalOxidative StressReceptor, Notch3SepsisBiomarkersFatty Acids, Omega-3MicroRNAsMirn1 microRNA, mouseReceptor, Notch3Smad ProteinsInflammationIntestinal injurymicroRNA-1-3pNotch3Omega-3 fatty acidsSepsisSmadStress oxidative

Identifiers

PMID35090386
PMCPMC8796544
OpenAlexW4210261554

What OpenQuestion 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 OpenQuestion graph.