Evidence map›Paper›PMID 38413746›Full record

ArticleNature chemical biology2024

Adipose triglyceride lipase suppresses noncanonical inflammasome by hydrolyzing LPS.

Weitao Li, Qiannv Liu, Yan Qian, Chunlei Wang, Chun Kong, Liangliang Sun, Li Sun, Hongwei Liu, Yan Zhang, Dong Jiang and 3 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature chemical biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

5 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Review
  3. Bilirubin Targeting WNK1 to Alleviate NLRP3-Mediated Neuroinflammation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  4. Article
  5. 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

13 authors at 3 institutions in 1 country.

Weitao Li *Department of Immunology, School of Basic Medical Sciences, Peking University, Beijing, China.
Qiannv Liu *Department of Immunology, School of Basic Medical Sciences, Peking University, Beijing, China.
Yan QianDepartment of Immunology, School of Basic Medical Sciences, Peking University, Beijing, China.
Chunlei WangDepartment of Immunology, School of Basic Medical Sciences, Peking University, Beijing, China.
Chun KongDepartment of Immunology, School of Basic Medical Sciences, Peking University, Beijing, China.
Liangliang SunDepartment of Immunology, School of Basic Medical Sciences, Peking University, Beijing, China.
Li SunState Key Laboratory of Mycology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, China.
Hongwei LiuState Key Laboratory of Mycology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, China.
Yan ZhangDepartment of Immunology, School of Basic Medical Sciences, Peking University, Beijing, China.
Dong JiangDepartment of Sports Medicine, Peking University Third Hospital, Beijing, China.
Changtao JiangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, China.
Shuo WangCAS Key Laboratory of Pathogen Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, China.
Pengyan XiaDepartment of Immunology, School of Basic Medical Sciences, Peking University, Beijing, China. xiap@pku.edu.cn.ORCID http://orcid.org/0000-0001-7959-5796
Chinese Academy of Medical Sciences & Peking Union Medical College · CNChinese Academy of Sciences · CNPeking University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 31925021National Natural Science Foundation of China (National Science Foundation of China) 82271790National Natural Science Foundation of China (National Science Foundation of China) 92169113National Natural Science Foundation of China (National Science Foundation of China) 92369104Natural Science Foundation of Beijing Municipality (Beijing Natural Science Foundation) 7212067Natural Science Foundation of Beijing Municipality (Beijing Natural Science Foundation) JQ23028
6 · The paper itself

Abstract

Intracellular recognition of lipopolysaccharide (LPS) by mouse caspase-11 or human caspase-4 is a vital event for the activation of the noncanonical inflammasome. Whether negative regulators are involved in intracellular LPS sensing is still elusive. Here we show that adipose triglyceride lipase (ATGL) is a negative regulator of the noncanonical inflammasome. Through screening for genes participating in the noncanonical inflammasome, ATGL is identified as a negative player for intracellular LPS signaling. ATGL binds LPS and catalyzes the removal of the acylated side chains that contain ester bonds. LPS with under-acylated side chains no longer activates the inflammatory caspases. Cells with ATGL deficiency exhibit enhanced immune responses when encountering intracellular LPS, including an elevated secretion of interleukin-1β, decreased cell viability and increased cell cytotoxicity. Moreover, ATGL-deficient mice show exacerbated responses to endotoxin challenges. Our results uncover that ATGL degrades cytosolic LPS to suppress noncanonical inflammasome activation.

Indexed as

InflammasomesLipaseLipopolysaccharidesAcyltransferasesAnimalsCaspases, InitiatorCell SurvivalHumansHydrolysisInterleukin-1betaMiceMice, Inbred C57BLMice, KnockoutAcyltransferasesCasp4 protein, mouseCaspases, InitiatorInflammasomesInterleukin-1betaLipaseLipopolysaccharidesPNPLA2 protein, humanPNPLA2 protein, mouse

Identifiers

PMID38413746
OpenAlexW4392192943

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.