Evidence map›Paper›PMID 39455437›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2024

The role of Gαq in regulating NLRP3 inflammasome activation.

Ruixue Kong, Lijun Peng, Honggang Bao, Lulu Sun, Yan Feng, Hua Li, Dashan Wang

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

2 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
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

7 authors.

Ruixue KongCollege of Life Sciences, Shandong Normal University, Jinan, 250014, Shandong, China.
Lijun PengDepartment of Gastroenterology, Linyi People's Hospital, Linyi, 276000, Shandong, China.
Honggang BaoDepartment of Laboratory Medicine, Linyi Cancer Hospital, Linyi, 276000, Shandong, China.
Lulu SunCollege of Life Sciences, Shandong Normal University, Jinan, 250014, Shandong, China.
Yan FengCollege of Life Sciences, Shandong Normal University, Jinan, 250014, Shandong, China.
Hua LiCollege of Life Sciences, Shandong Normal University, Jinan, 250014, Shandong, China. lihua@sdnu.edu.cn.
Dashan WangResearch Center, Shandong Medical College, Linyi, 276000, Shandong, China. wds1055@163.com.

Funding

National Natural Science Foundation of China 81871308Shandong Province Higher Educational Science and Technology Program J18KA259Shandong Province Higher Educational Youth Scientific Research Innovation Team Program 2019KJK018Shandong Provincial Natural Science Foundation Project ZR2019QH002
6 · The paper itself

Abstract

backgroundG proteins are a class of important signal transducers in mammalians. G proteins can corpoarated with G proteincoupled receptors (GPCRs) and transmit signals from extracellular stimuli into intracellular response, which will regulate a series of biological functions. G-proteins are heterotrimeric proteins composed of Gα, Gβ, and Gγ subunits. Based on structural and functional similarity of their α-subunits, G proteins are typically grouped into four classes (Gi, Gs, Gq/11, and G12/13). The Gq/11 subfamily consists of Gq, G11, G14, and G15/16 proteins. Gαq is the α-subunit of Gq protein and encoded by GNAQ. Our previous studies revealed that Gαq play an important role in regulating T cell survival and T cell differentiation. Inflammasomes are multiprotein complexes that play a critical role in modulating innate inflammatory response. NLRP3 inflammasome is currently the most extensively studied inflammasome.

methodsWe found that Gαq suppressed NLRP3 inflammasome activation in macrophage, Gαq also suppressed NLRP3 inflammasome activation in a LPS-induced sepsis mouse model. Gαq can locate to mitochondria and Gαq was required for the maintenance of mitochondrial homeostasis. Gαq regulated NLRP3 inflammasome activation by modulating mitochondrial reactive oxygen species (mtROS).

resultsWe found that Gαq suppressed NLRP3 inflammasome activation in macrophage, Gαq also suppressed NLRP3 inflammasome activation in a LPS-induced sepsis mouse model. Gαq can locate to mitochondria and Gαq was required for the maintenance of mitochondrial homeostasis. Gαq regulated NLRP3 inflammasome activation by modulating mitochondrial reactive oxygen species (mtROS).

conclusionOur results indicate that Gαq regulates NLRP3 inflammasome activation by modulating mitochondrial ROS production. Our research provides new mechanistic insight into the activation of NLRP3 inflammasome. As it has been proved that NLRP3 inflammasome plays an important role in the pathogenesis many diseases such as Alzheimer's disease, cancer, and inflammatory bowel disease, Gαq might become a novel drug target for these diseases in future.

Indexed as

GTP-Binding Protein alpha Subunits, Gq-G11InflammasomesLipopolysaccharidesMice, Inbred C57BLNLR Family, Pyrin Domain-Containing 3 ProteinAnimalsHumansMacrophagesMaleMiceMitochondriaRAW 264.7 CellsReactive Oxygen SpeciesSepsisGTP-Binding Protein alpha Subunits, Gq-G11InflammasomesLipopolysaccharidesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseReactive Oxygen SpeciesG-proteinsGαqMitochondriaNLRP3 inflammasomeReactive oxygen species

Identifiers

PMID39455437

What Socratic holds

Textmetadata
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 Socratic graph.