Evidence map›Paper›PMID 37864659›Full record

ArticleInflammation2024

Fibroblast Growth Factor 21 Relieves Lipopolysaccharide-Induced Acute Lung Injury by Suppressing JAK2/STAT3 Signaling Pathway.

Mengsi Cai, Huihui Ye, Xiayan Zhu, Xiuchun Li, Luqiong Cai, Jiajia Jin, Qiwen Chen, Yuzhe Shi, Lehe Yang, Liangxing Wang and 1 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Inflammation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
2.5field-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

7 citing papers in PubMed, 16 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

11 authors at 1 institution in 1 country.

Mengsi CaiDivision of Pulmonary Medicine, the First Affiliated Hospital, Wenzhou Medical University, Wenzhou Key Laboratory Interdiscipline and Translational Medicine, Wenzhou Key Laboratory of Heart and Lung, Wenzhou Medical University, Xuefu North Street, Wenzhou, Zhejiang, 325000, People's Republic of China.
Huihui YeDivision of Pulmonary Medicine, the First Affiliated Hospital, Wenzhou Medical University, Wenzhou Key Laboratory Interdiscipline and Translational Medicine, Wenzhou Key Laboratory of Heart and Lung, Wenzhou Medical University, Xuefu North Street, Wenzhou, Zhejiang, 325000, People's Republic of China.
Xiayan ZhuDivision of Pulmonary Medicine, the First Affiliated Hospital, Wenzhou Medical University, Wenzhou Key Laboratory Interdiscipline and Translational Medicine, Wenzhou Key Laboratory of Heart and Lung, Wenzhou Medical University, Xuefu North Street, Wenzhou, Zhejiang, 325000, People's Republic of China.
Xiuchun LiDivision of Pulmonary Medicine, the First Affiliated Hospital, Wenzhou Medical University, Wenzhou Key Laboratory Interdiscipline and Translational Medicine, Wenzhou Key Laboratory of Heart and Lung, Wenzhou Medical University, Xuefu North Street, Wenzhou, Zhejiang, 325000, People's Republic of China.
Luqiong CaiDivision of Pulmonary Medicine, the First Affiliated Hospital, Wenzhou Medical University, Wenzhou Key Laboratory Interdiscipline and Translational Medicine, Wenzhou Key Laboratory of Heart and Lung, Wenzhou Medical University, Xuefu North Street, Wenzhou, Zhejiang, 325000, People's Republic of China.
Jiajia JinDivision of Pulmonary Medicine, the First Affiliated Hospital, Wenzhou Medical University, Wenzhou Key Laboratory Interdiscipline and Translational Medicine, Wenzhou Key Laboratory of Heart and Lung, Wenzhou Medical University, Xuefu North Street, Wenzhou, Zhejiang, 325000, People's Republic of China.
Qiwen ChenThe First Clinical Medical College, Wenzhou Medical University, Wenzhou, Zhejiang, 325000, People's Republic of China.
Yuzhe ShiThe First Clinical Medical College, Wenzhou Medical University, Wenzhou, Zhejiang, 325000, People's Republic of China.
Lehe YangDivision of Pulmonary Medicine, the First Affiliated Hospital, Wenzhou Medical University, Wenzhou Key Laboratory Interdiscipline and Translational Medicine, Wenzhou Key Laboratory of Heart and Lung, Wenzhou Medical University, Xuefu North Street, Wenzhou, Zhejiang, 325000, People's Republic of China.
Liangxing WangDivision of Pulmonary Medicine, the First Affiliated Hospital, Wenzhou Medical University, Wenzhou Key Laboratory Interdiscipline and Translational Medicine, Wenzhou Key Laboratory of Heart and Lung, Wenzhou Medical University, Xuefu North Street, Wenzhou, Zhejiang, 325000, People's Republic of China. zjwzhxy@126.com.
Xiaoying HuangDivision of Pulmonary Medicine, the First Affiliated Hospital, Wenzhou Medical University, Wenzhou Key Laboratory Interdiscipline and Translational Medicine, Wenzhou Key Laboratory of Heart and Lung, Wenzhou Medical University, Xuefu North Street, Wenzhou, Zhejiang, 325000, People's Republic of China. huangxiaoying@wzhospital.cn.
Wenzhou Medical University · CN

Funding

Science and Technology Plan Project of Wenzhou, China 2020ZY0036Zhejiang Xinmiao Talents Program 2022R413A040
6 · The paper itself

Abstract

Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a life-threatening disease without an effective drug at present. Fibroblast growth factor 21 (FGF21) was reported to be protective against inflammation in metabolic disease in recent studies. However, the role of FGF21 in ALI has been rarely investigated. In this study, it was found that the expression of FGF21 was markedly increased in lung tissue under lipopolysaccharide (LPS) stimulation in vivo, whereas it was decreased in lung epithelial cells under LPS stimulation in vitro. Therefore, our research aimed to elucidate the potential role of FGF21 in LPS-induced ALI and to detect possible underlying mechanisms. The results revealed that the deficiency of FGF21 aggravated pathological damage, inflammatory infiltration, and pulmonary function in LPS-induced ALI, while exogenous administration of FGF21 improved these manifestations. Moreover, through RNA sequencing and enrichment analysis, it was unveiled that FGF21 might play a protective role in LPS-induced ALI via JAK2/STAT3 signaling pathway. The therapeutic effect of FGF21 was weakened after additional usage of JAK2 activator in vivo. Further investigation revealed that FGF21 significantly inhibited STAT3 phosphorylation and impaired the nuclear translocation of STAT3 in vitro. In addition, the aggravation of inflammation caused by silencing FGF21 can be alleviated by JAK2 inhibitor in vitro. Collectively, these findings unveil a potent protective effect of FGF21 against LPS-induced ALI by inhibiting the JAK2/STAT3 pathway, implying that FGF21 might be a novel and effective therapy for ALI.

Indexed as

Acute Lung InjuryFibroblast Growth FactorsRespiratory Distress SyndromeHumansInflammationJanus Kinase 2LipopolysaccharidesLungSignal TransductionSTAT3 Transcription FactorFGF21 protein, humanfibroblast growth factor 21Fibroblast Growth FactorsJAK2 protein, humanJanus Kinase 2LipopolysaccharidesSTAT3 protein, humanSTAT3 Transcription FactorAcute lung injury (ALI)/acute respiratory distress syndrome (ARDS)FGF21JAK2/STAT3 signal pathway.

Identifiers

PMID37864659
PMCPMC10799097
OpenAlexW4387845325

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.