Evidence map›Paper›PMID 39753529›Full record

ArticleNature communications2025

Macrophage STING signaling promotes fibrosis in benign airway stenosis via an IL6-STAT3 pathway.

YiLin Chen, ChengCheng Yang, YuShan Miao, DongChen Shi, Xiang Li, Sen Tian, YiFei Zhang, ChengFei Xu, YuChao Dong, ChaoFeng Han and 2 more

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
–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

29 citing papers in PubMed.

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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

12 authors.

YiLin Chen *Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Naval Medical University, Shanghai, China.
ChengCheng Yang *Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Naval Medical University, Shanghai, China.
YuShan Miao *Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Naval Medical University, Shanghai, China.
DongChen ShiDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Naval Medical University, Shanghai, China.
Xiang LiDepartment of Respiratory and Critical Care Medicine, General Hospital of Central Theater Command of Chinese People's Liberation Army, Wuhan, China.
Sen TianDepartment of Respiratory and Critical Care Medicine, No. 906 Hospital of the Chinese People's Liberation Army Joint Logistic Support Force, Ningbo, China.
YiFei ZhangDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Naval Medical University, Shanghai, China.
ChengFei XuDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Naval Medical University, Shanghai, China.
YuChao DongDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Naval Medical University, Shanghai, China.
ChaoFeng HanDepartment of Histology and Embryology, Naval Medical University, Shanghai, China. hcf@immunol.org.ORCID 0000-0002-8489-6478
Hui ShiDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Naval Medical University, Shanghai, China. Shihui@smmu.edu.cn.ORCID 0009-0009-6676-1834
Chong BaiDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Naval Medical University, Shanghai, China. Chongbai@smmu.edu.cn.ORCID 0000-0003-2039-5751

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82270112National Science Foundation of China | Young Scientists Fund 82000102
6 · The paper itself

Abstract

Acute and chronic inflammation are important pathologies of benign airway stenosis (BAS) fibrosis, which is a frequent complication of critically ill patients. cGAS-STING signalling has an important role in inflammation and fibrosis, yet the function of STING in BAS remains unclear. Here we demonstrate using scRNA sequencing that cGAS‒STING signalling is involved in BAS, which is accompanied by increased dsDNA, expression and activation of STING. STING inhibition or deficiency effectively alleviates tracheal fibrosis of BAS mice by decreasing both acute and chronic inflammation. Macrophage depletion also effectively ameliorates BAS. Mechanistically, dsDNA from damaged epithelial cells activates the cGAS-STING pathway of macrophages and induces IL-6 to activate STAT3 and promote fibrosis. In summary, the present results suggest that cGAS-STING signalling induces acute inflammation and amplifies the chronic inflammation and tracheal fibrosis associated with benign airway stenosis, highlighting the mechanism and potential drug target of BAS.

Indexed as

FibrosisInterleukin-6MacrophagesMembrane ProteinsSignal TransductionSTAT3 Transcription FactorAnimalsCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseDisease Models, AnimalDNAEpithelial CellsFemaleHumansInflammationMaleMicecGAS protein, mouseCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseDNAInterleukin-6Membrane ProteinsNucleotidyltransferasesStat3 protein, mouseSTAT3 Transcription FactorSting1 protein, mouseSTING Protein

Identifiers

PMID39753529
PMCPMC11698984

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.