Evidence map›Paper›PMID 30126430›Full record

ArticleJournal of translational medicine2018

RIP3 dependent NLRP3 inflammasome activation is implicated in acute lung injury in mice.

Jingxian Chen, Shuang Wang, Rong Fu, Mianjing Zhou, Tengyue Zhang, Wenxu Pan, Niansheng Yang, Yuefang Huang

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
3.4field-weighted citation impact, top 6% 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

49 citing papers in PubMed, 102 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

8 authors at 2 institutions in 1 country.

Jingxian ChenDepartment of Pediatrics, First Affiliated Hospital, Sun Yat-sen University, 58 Zhongshan Road II, Guangzhou, 510080, People's Republic of China.
Shuang WangDepartment of Rheumatology, First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080, People's Republic of China.
Rong FuDepartment of Rheumatology, Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, 510260, People's Republic of China.
Mianjing ZhouDepartment of Rheumatology, First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080, People's Republic of China.
Tengyue ZhangDepartment of Pediatrics, First Affiliated Hospital, Sun Yat-sen University, 58 Zhongshan Road II, Guangzhou, 510080, People's Republic of China.
Wenxu PanDepartment of Pediatrics, First Affiliated Hospital, Sun Yat-sen University, 58 Zhongshan Road II, Guangzhou, 510080, People's Republic of China.
Niansheng YangDepartment of Rheumatology, First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080, People's Republic of China.
Yuefang HuangDepartment of Pediatrics, First Affiliated Hospital, Sun Yat-sen University, 58 Zhongshan Road II, Guangzhou, 510080, People's Republic of China. zsuhyf@163.com.ORCID 0000-0003-2742-3583
Sun Yat-sen University · CNSecond Affiliated Hospital of Guangzhou Medical University · CN

Funding

Guangdong Science and Technology Planning Program 2013B021800113Guangdong Science and Technology Planning Program 201707010093National Natural Science Foundation of China 81471598National Natural Science Foundation of China 81671593National Natural Science Foundation of China 81701595Natural Science Foundation of Guangdong Province 2016A030310172
6 · The paper itself

Abstract

backgroundNLRP3 inflammasome is involved in the inflammatory responses during acute lung injury (ALI). RIP3 triggered NLRP3 inflammasome activation independent of necroptosis induction has recently been documented. In this study, the role of RIP3 in the activation of NLRP3 inflammasome in the development of ALI was investigated.

methodsA selective RIP3 inhibitor GSK872 was used to investigate the roles of RIP3 in NLRP3 inflammasome activation in the lipopolysaccharide (LPS) induced ALI mouse model. The mechanism of NLRP3 inflammasome activation was investigated in the human monocytic cell line THP-1. NLRP3 inflammasome and necroptosis were measured by flow cytometry or western blot. RIP3-NLRP3 interaction was interrogated using immunoprecipitation and the Duolink

resultsSignificant upregulation of both necroptosis and NLRP3 inflammasome pathways were observed in the lungs of mice with LPS induced ALI. GSK872 significantly suppressed the activation of necroptosis and NLRP3 activation with reduction of IL-1β and IL-18 production and inflammatory cells infiltration, resulting in a significant amelioration of lung injury. These two processes were shown to be active in interstitial macrophages and CD11b

conclusionTaking together, these results show that RIP3 participates in the NLRP3 inflammasome activation in infiltrating macrophages in ALI induced by LPS. This process plays a significant pathogenic role in LPS-induced lung injury.

Indexed as

Acute Lung InjuryAnimalsApoptosisBenzothiazolesCell LineEnzyme InhibitorsInflammasomesInflammationLipopolysaccharidesMaleMiceMice, Inbred C57BLMonocytesNecrosisNLR Family, Pyrin Domain-Containing 3 ProteinQuinolinesBenzothiazolesEnzyme InhibitorsGSK872InflammasomesLipopolysaccharidesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseQuinolinesReceptor-Interacting Protein Serine-Threonine KinasesRipk3 protein, mouseAcute lung injuryIL-1βInflammasomeNecroptosisRIP3

Identifiers

PMID30126430
PMCPMC6102827
OpenAlexW2888323682

What OpenQuestion holds

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Registered trials

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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.