Evidence map›Paper›PMID 30940803›Full record

ArticleNature communications2019

The lncRNA Neat1 promotes activation of inflammasomes in macrophages.

Pengfei Zhang, Limian Cao, Rongbin Zhou, Xiaolu Yang, Mian Wu

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 293 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
293citing papers in PubMed, 2 pooled it
24.2field-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

293 citing papers in PubMed, 2 syntheses or guidelines pooled it, 497 citations in OpenAlex.

  1. Pooled it
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  15. mRedox biology · 2026
    Review
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233 more citing papers are in PubMed but not listed here.

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 3 institutions in 2 countries.

Pengfei ZhangThe Chinese Academy of Sciences (CAS) Key Laboratory of Innate Immunity and Chronic Disease, CAS Center for Excellence in Cell and Molecular Biology, School of Life Sciences, University of Science and Technology of China, 230026, Hefei, China.
Limian CaoThe Chinese Academy of Sciences (CAS) Key Laboratory of Innate Immunity and Chronic Disease, CAS Center for Excellence in Cell and Molecular Biology, School of Life Sciences, University of Science and Technology of China, 230026, Hefei, China.
Rongbin ZhouThe Chinese Academy of Sciences (CAS) Key Laboratory of Innate Immunity and Chronic Disease, CAS Center for Excellence in Cell and Molecular Biology, School of Life Sciences, University of Science and Technology of China, 230026, Hefei, China.ORCID http://orcid.org/0000-0002-3351-6420
Xiaolu YangDepartment of Cancer Biology and Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA. xyang@mail.med.upenn.edu.
Mian WuThe Chinese Academy of Sciences (CAS) Key Laboratory of Innate Immunity and Chronic Disease, CAS Center for Excellence in Cell and Molecular Biology, School of Life Sciences, University of Science and Technology of China, 230026, Hefei, China. wumian@ustc.edu.cn.
University of Science and Technology of China · CNCancer Research Institute · USHenan University · CN

Funding

p53 and tumor cell metabolismR01CA182675 · NCI · UNIVERSITY OF PENNSYLVANIA · PI YANG, XIAOLU · 2014 to 2018
$1.7M
Role of p53 family proteins in glucose metabolismR01CA184867 · NCI · UNIVERSITY OF PENNSYLVANIA · PI YANG, XIAOLU · 2014 to 2017
$1.3M
NCI NIH HHS R01 CA182675NCI NIH HHS R01 CA184867NIH HHS R01CA182675NIH HHS R01CA184867
6 · The paper itself

Abstract

The inflammasome has an essential function in innate immune, responding to a wide variety of stimuli. Here we show that the lncRNA Neat1 promotes the activation of several inflammasomes. Neat1 associates with the NLRP3, NLRC4, and AIM2 inflammasomes in mouse macrophages to enhance their assembly and subsequent pro-caspase-1 processing. Neat1 also stabilizes the mature caspase-1 to promote interleukin-1β production and pyroptosis. Upon stimulation with inflammasome-activating signals, Neat1, which normally resides in the paraspeckles, disassociates from these nuclear bodies and translocates to the cytoplasm to modulate inflammasome activation using above mechanism. Neat1 is also up-regulated under hypoxic conditions in a HIF-2α-dependent manner, mediating the effect of hypoxia on inflammasomes. Moreover, in the mouse models of peritonitis and pneumonia, Neat1 deficiency significantly reduces inflammatory responses. These results reveal a previously unrecognized role of lncRNAs in innate immunity, and suggest that Neat1 is a common mediator for inflammasome stimuli.

Indexed as

AnimalsApoptosis Regulatory ProteinsBasic Helix-Loop-Helix ProteinsCalcium-Binding ProteinsCaspase 1Cells, CulturedDNA-Binding ProteinsEndothelial PAS Domain-Containing Protein 1FemaleHumansInflammasomesInflammationInterleukin-1betaMacrophagesMaleMiceAim2 protein, mouseApoptosis Regulatory ProteinsBasic Helix-Loop-Helix ProteinsCalcium-Binding ProteinsCaspase 1DNA-Binding ProteinsEndothelial PAS Domain-Containing Protein 1InflammasomesInterleukin-1betaIpaf protein, mouseNEAT1 long non-coding RNA, mouseNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseRNA, Long Noncoding

Identifiers

PMID30940803
PMCPMC6445148
OpenAlexW2926902798

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.