Evidence map›Paper›PMID 34783310›Full record

ArticleeLife2021

A highly conserved host lipase deacylates oxidized phospholipids and ameliorates acute lung injury in mice.

Benkun Zou, Michael Goodwin, Danial Saleem, Wei Jiang, Jianguo Tang, Yiwei Chu, Robert S Munford, Mingfang Lu

Open access · goldAbstract read
In one paragraph

Article in eLife, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

9 citing papers in PubMed, 11 citations in OpenAlex.

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  5. Chick early amniotic fluid attenuates lipopolysaccharide-induced acute lung injury.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
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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 1 institution in 1 country.

Benkun ZouDepartment of Immunology, Key Laboratory of Medical Molecular Virology (MOE, NHC, CAMS), School of Basic Medical Sciences & Shanghai Institute of Infectious Disease and Biosecurity, Fudan University, Shanghai, China.ORCID 0000-0002-6980-0909
Michael GoodwinLaboratory of Clinical Immunology and Microbiology, NIAID, NIH, Bethesda, United States.
Danial SaleemLaboratory of Clinical Immunology and Microbiology, NIAID, NIH, Bethesda, United States.ORCID 0000-0003-2310-6062
Wei JiangDepartment of Immunology, Key Laboratory of Medical Molecular Virology (MOE, NHC, CAMS), School of Basic Medical Sciences & Shanghai Institute of Infectious Disease and Biosecurity, Fudan University, Shanghai, China.
Jianguo TangDepartment of Trauma-Emergency & Critical Care Medicine, Shanghai Fifth People's Hospital, Fudan University, Shanghai, China.
Yiwei ChuDepartment of Immunology, Key Laboratory of Medical Molecular Virology (MOE, NHC, CAMS), School of Basic Medical Sciences & Shanghai Institute of Infectious Disease and Biosecurity, Fudan University, Shanghai, China.
Robert S MunfordLaboratory of Clinical Immunology and Microbiology, NIAID, NIH, Bethesda, United States.ORCID 0000-0003-1509-1294
Mingfang LuDepartment of Immunology, Key Laboratory of Medical Molecular Virology (MOE, NHC, CAMS), School of Basic Medical Sciences & Shanghai Institute of Infectious Disease and Biosecurity, Fudan University, Shanghai, China.ORCID 0000-0002-8612-3444
Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidized phospholipids have diverse biological activities, many of which can be pathological, yet how they are inactivated in vivo is not fully understood. Here, we present evidence that a highly conserved host lipase, acyloxyacyl hydrolase (AOAH), can play a significant role in reducing the pro-inflammatory activities of two prominent products of phospholipid oxidation, 1-palmitoyl-2-glutaryl-sn-glycero-3-phosphocholine and 1-palmitoyl-2-(5-oxovaleroyl)-sn-glycero-3-phosphocholine. AOAH removed the sn-2 and sn-1 acyl chains from both lipids and reduced their ability to induce macrophage inflammasome activation and cell death in vitro and acute lung injury in mice. In addition to transforming Gram-negative bacterial lipopolysaccharide from stimulus to inhibitor, its most studied activity, AOAH can inactivate these important danger-associated molecular pattern molecules and reduce tissue inflammation and injury.

Indexed as

Acute Lung InjuryAnimalsCarboxylic Ester HydrolasesCells, CulturedHydrochloric AcidInflammasomesInflammationLipopolysaccharidesMacrophagesMiceMice, TransgenicOxidation-ReductionPhospholipidsacyloxyacyl hydrolaseCarboxylic Ester HydrolasesHydrochloric AcidInflammasomesLipopolysaccharidesPhospholipidsacute lung injuryacyloxyacyl hydrolaseimmunologyinflammasomeinflammationmacrophagemouseoxidized phospholipid

Identifiers

PMID34783310
PMCPMC8594946
OpenAlexW3213410746

What OpenQuestion holds

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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.