Evidence map›Paper›PMID 32089649›Full record

ArticleMediators of inflammation2020

Depression of lncRNA NEAT1 Antagonizes LPS-Evoked Acute Injury and Inflammatory Response in Alveolar Epithelial Cells via HMGB1-RAGE Signaling.

Hongchao Zhou, Xinhui Wang, Bin Zhang

Open access · goldAbstract read
In one paragraph

Article in Mediators of inflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
8.6field-weighted citation impact, top 1% 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

53 citing papers in PubMed, 81 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

3 authors at 2 institutions in 1 country.

Hongchao ZhouDepartment of Intensive Care Units, Zhoukou Central Hospital, Zhoukou, Henan 466000, China.ORCID https://orcid.org/0000-0002-4506-7554
Xinhui WangDepartment of Intensive Care Units, Zhoukou Central Hospital, Zhoukou, Henan 466000, China.ORCID https://orcid.org/0000-0003-3191-8271
Bin ZhangDepartment of General Surgery, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, Henan 453100, China.ORCID https://orcid.org/0000-0002-4684-3789
Zhoukou Normal University · CNFirst Affiliated Hospital of Xinxiang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sepsis-evoked acute lung injury (ALI) and its extreme manifestation, acute respiratory distress syndrome (ARDS), constitute a major cause of mortality in intensive care units. High levels of the long noncoding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) have been positively correlated with increased severity and unfavorable prognoses in patients with sepsis. Nevertheless, the function and molecular mechanism of NEAT1 in ALI remain elusive. In the current study, high levels of NEAT1 were confirmed in lipopolysaccharide- (LPS-) induced ALI mice models and in LPS-stimulated cells from the alveolar epithelial A549 cell line. Intriguingly, cessation of NEAT1 led to increased cell viability and decreased lactate dehydrogenase release, apoptosis, and caspase-3/9 activity, which conferred protection against LPS-induced injury in these cells. NEAT1 inhibition also restrained LPS-evoked transcripts and production of inflammatory cytokines IL-6, IL-1

Indexed as

A549 CellsAlveolar Epithelial CellsAnimalsHMGB1 ProteinHumansInterleukin-1betaInterleukin-6LentivirusLipopolysaccharidesMaleMiceMice, Inbred C57BLReceptor for Advanced Glycation End ProductsRNA, Long NoncodingSignal TransductionTumor Necrosis Factor-alphaHMGB1 ProteinInterleukin-1betaInterleukin-6LipopolysaccharidesNEAT1 long non-coding RNA, humanReceptor for Advanced Glycation End ProductsRNA, Long NoncodingTumor Necrosis Factor-alpha

Identifiers

PMID32089649
PMCPMC7025070
OpenAlexW3004871257

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.