Evidence map›Paper›PMID 32795289›Full record

ArticleRespiratory research2020

HGF alleviates septic endothelial injury by inhibiting pyroptosis via the mTOR signalling pathway.

Fei Peng, Wei Chang, Qin Sun, Xinyi Xu, Jianfeng Xie, Haibo Qiu, Yi Yang

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

24 citing papers in PubMed, 37 citations in OpenAlex.

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  13. O-GlcNAc modification of GSDMD attenuates LPS-induced endothelial cells pyroptosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
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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

7 authors at 1 institution in 1 country.

Fei PengJiangsu Provincial Key Laboratory of Critical Care Medicine, Department of Critical Care Medicine, Zhongda Hospital, School of Medicine, Southeast University, 87 Dingjiaqiao Rd, Nanjing, 210009, People's Republic of China.
Wei ChangJiangsu Provincial Key Laboratory of Critical Care Medicine, Department of Critical Care Medicine, Zhongda Hospital, School of Medicine, Southeast University, 87 Dingjiaqiao Rd, Nanjing, 210009, People's Republic of China.
Qin SunJiangsu Provincial Key Laboratory of Critical Care Medicine, Department of Critical Care Medicine, Zhongda Hospital, School of Medicine, Southeast University, 87 Dingjiaqiao Rd, Nanjing, 210009, People's Republic of China.
Xinyi XuJiangsu Provincial Key Laboratory of Critical Care Medicine, Department of Critical Care Medicine, Zhongda Hospital, School of Medicine, Southeast University, 87 Dingjiaqiao Rd, Nanjing, 210009, People's Republic of China.
Jianfeng XieJiangsu Provincial Key Laboratory of Critical Care Medicine, Department of Critical Care Medicine, Zhongda Hospital, School of Medicine, Southeast University, 87 Dingjiaqiao Rd, Nanjing, 210009, People's Republic of China.
Haibo QiuJiangsu Provincial Key Laboratory of Critical Care Medicine, Department of Critical Care Medicine, Zhongda Hospital, School of Medicine, Southeast University, 87 Dingjiaqiao Rd, Nanjing, 210009, People's Republic of China.
Yi YangJiangsu Provincial Key Laboratory of Critical Care Medicine, Department of Critical Care Medicine, Zhongda Hospital, School of Medicine, Southeast University, 87 Dingjiaqiao Rd, Nanjing, 210009, People's Republic of China. yiyiyang2004@163.com.ORCID https://orcid.org/0000-0003-1661-3568
Zhongda Hospital Southeast University · CN

Funding

Jiangsu Province's Key Discipline / Laboratory of Medicine ZDXKA2016025Jiangsu Province's Key Provincial Talents Program ZDRCA2016082National Natural Science Foundation of China 81671892, 81971888National Science and Technology Major Project for Control and Prevention of Major Infectious Diseases of China 2017ZX10103004Natural Science Foundation of Jiangsu Province BK20161433Postgraduate Research & Practice Innovation Program of Jiangsu Province KYCX18_0181
6 · The paper itself

Abstract

backgroundEndothelial injury is one of the predominant pathophysiological characteristics of sepsis and is the major cause of sepsis-induced multiple organ failure. Endothelial pyroptosis is a fatal mechanism of endothelial injury in sepsis, and specific, effective therapies are lacking. Although hepatocyte growth factor (HGF) has been shown to have anti-apoptotic and anti-necrotic effects, whether it prevents pyroptosis to improve endothelial injury in sepsis remains unclear.

methodsRecombinant HGF was intravenously injected into mice with sepsis caused by caecal ligation puncture (CLP). Histopathological examination and transmission electron microscopy (TEM) were used to measure lung vascular endothelial injury. Lipopolysaccharide (LPS) was transfected into EA.hy926 cells to induce endothelial pyroptosis, and the cells were treated with HGF in the presence of inhibitors of c-Met and mTOR, namely, PHA-665752 and rapamycin, respectively. The mTOR signalling pathway and mitochondrial physiology were assessed using Western blot and flow cytometry.

resultsIntravenous HGF effectively alleviated pulmonary vascular endothelial injury and acute lung injury in the septic mice. The TEM results of lung tissue revealed that HGF attenuated pulmonary vascular endothelial pyroptosis, which was confirmed in vitro. Transfected LPS induced the pyroptosis of EA.hy926 cells and damaged their paracellular permeability, and these effects were ameliorated by treating the cells with recombinant HGF. The protective effect of HGF against pyroptosis was dependent on c-Met/mTOR signalling. mTOR activation effectively protected mitochondrial physiology and decreased reactive oxygen species (ROS) production in EA.hy926 cells in vitro.

conclusionsThese results demonstrated that HGF protected mitochondrial physiology by activating mTOR signalling to partially ameliorate endothelial pyroptosis and attenuate vascular endothelial injury and acute lung injury in sepsis animal model.

Indexed as

Administration, IntravenousAnimalsCells, CulturedHepatocyte Growth FactorHumansMiceMice, Inbred C57BLPyroptosisSepsisSignal TransductionTOR Serine-Threonine KinasesHepatocyte Growth FactormTOR protein, mouseTOR Serine-Threonine KinasesEndothelial injuryHGFMitochondria physiologymTORPyroptosisSepsis

Identifiers

PMID32795289
PMCPMC7427898
OpenAlexW3049137160

What OpenQuestion holds

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LicenceCC BY
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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.