Evidence map›Paper›PMID 29845275›Full record

ArticleMolecular medicine reports2018

miR‑23a downregulation modulates the inflammatory response by targeting ATG12‑mediated autophagy.

Xiang Si, Daiyin Cao, Juan Chen, Yao Nie, Zhiyi Jiang, Min-Ying Chen, Jian-Feng Wu, Xiang-Dong Guan

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 27% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

  1. Pooled it
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  5. Molecular mechanism of miRNA-23a in sepsis-induced lung injury.American journal of translational research · 2023
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  17. Silencing of long non-coding RNA MALAT1 suppresses inflammation in septic mice: role of microRNA-23a in the down-regulation of MCEMP1 expression.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020
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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 3 institutions in 1 country.

Xiang SiDepartment of SICU, The First Affiliated Hospital of Sun Yat‑sen University, Guangzhou, Guangdong 510000, P.R. China.
Daiyin CaoDepartment of Critical Care Medicine, The Sixth Affiliated Hospital of Sun Yat‑sen University, Guangzhou, Guangdong 510000, P.R. China.
Juan ChenDepartment of SICU, The First Affiliated Hospital of Sun Yat‑sen University, Guangzhou, Guangdong 510000, P.R. China.
Yao NieDepartment of SICU, The First Affiliated Hospital of Sun Yat‑sen University, Guangzhou, Guangdong 510000, P.R. China.
Zhiyi JiangDepartment of SICU, The First Affiliated Hospital of Sun Yat‑sen University, Guangzhou, Guangdong 510000, P.R. China.
Min-Ying ChenDepartment of SICU, The First Affiliated Hospital of Sun Yat‑sen University, Guangzhou, Guangdong 510000, P.R. China.
Jian-Feng WuDepartment of SICU, The First Affiliated Hospital of Sun Yat‑sen University, Guangzhou, Guangdong 510000, P.R. China.
Xiang-Dong GuanDepartment of SICU, The First Affiliated Hospital of Sun Yat‑sen University, Guangzhou, Guangdong 510000, P.R. China.
The First Affiliated Hospital, Sun Yat-sen University · CNSun Yat-sen University · CNSixth Affiliated Hospital of Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy, part of the innate immune defense mechanisms, is activated during the initial phase of septic insult. Previous studies indicated that micro (mi)RNAs are additionally involved in the host response to sepsis; however, the association between miRNAs and autophagy during this process is not fully understood. To study the role of miRNA (miR)‑23a in autophagy initiated by sepsis, macrophages treated with lipopolysaccharides, in addition to blood samples from patients, were evaluated for miR‑23a expression levels. Cell viability, inflammatory mediators and autophagic markers were investigated following overexpression or inhibition of miR‑23a. The results suggested that miR‑23a was suppressed subsequent to septic insult, promoting autophagy and suppressing a hyper inflammatory response, leading to enhanced cell viability. A luciferase assay and western blot analysis confirmed ubiquitin‑like protein ATG12 to be the target of miR‑23a. The present study revealed that the downregulation of miR‑23a regulates an inflammatory response during septic insult via autophagy promotion.

Indexed as

AgedAnimalsAntagomirsAutophagyAutophagy-Related Protein 12Base SequenceCell SurvivalFemaleGene Expression RegulationGenes, ReporterHumansLipopolysaccharidesLuciferasesMaleMiceMicroRNAsAntagomirsATG12 protein, humanAutophagy-Related Protein 12LipopolysaccharidesLuciferasesMicroRNAsMIRN23a microRNA, humanOligoribonucleotides

Identifiers

PMID29845275
PMCPMC6072189
OpenAlexW2806928714

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.