Evidence map›Paper›PMID 41254304›Full record

ArticleLung2025

Fibrinogen Gamma Chain Mediates Airway Inflammation and Remodeling Through the Focal Adhesion and TGF-β/Smad2 Pathways in Chronic Obstructive Pulmonary Disease.

Jiali Weng, Hai Zhang, Qing Chang, Yi Feng, Meiqin Xie, Chenfei Li, Qi Liu, Xiaohui Wang, Mengnan Li, Yuqing Chen and 4 more

Abstract read
PubMed Publisher
In one paragraph

Article in Lung, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

14 authors.

Jiali Weng *Department of Pulmonary and Critical Care Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, NO.241, West Huaihai Road, Shanghai, 200030, People's Republic of China.
Hai Zhang *Department of Pulmonary and Critical Care Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, NO.241, West Huaihai Road, Shanghai, 200030, People's Republic of China.
Qing ChangDepartment of Pulmonary and Critical Care Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, NO.241, West Huaihai Road, Shanghai, 200030, People's Republic of China.
Yi FengDepartment of Pulmonary and Critical Care Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, NO.241, West Huaihai Road, Shanghai, 200030, People's Republic of China.
Meiqin XieDepartment of Pulmonary and Critical Care Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, NO.241, West Huaihai Road, Shanghai, 200030, People's Republic of China.
Chenfei LiDepartment of Pulmonary and Critical Care Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, NO.241, West Huaihai Road, Shanghai, 200030, People's Republic of China.
Qi LiuDepartment of Pulmonary and Critical Care Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, NO.241, West Huaihai Road, Shanghai, 200030, People's Republic of China.
Xiaohui WangDepartment of Pulmonary and Critical Care Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, NO.241, West Huaihai Road, Shanghai, 200030, People's Republic of China.
Mengnan LiDepartment of Pulmonary and Critical Care Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, NO.241, West Huaihai Road, Shanghai, 200030, People's Republic of China.
Yuqing ChenDepartment of Pulmonary and Critical Care Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, NO.241, West Huaihai Road, Shanghai, 200030, People's Republic of China.
Chunhua LingDepartment of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Soochow University, Suzhou, 215000, People's Republic of China.
Kai WangDepartment of Central Laboratory, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, People's Republic of China.
Xiaohua YangDepartment of Central Laboratory, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, People's Republic of China.
Feng LiDepartment of Pulmonary and Critical Care Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, NO.241, West Huaihai Road, Shanghai, 200030, People's Republic of China. lifeng741@aliyun.com.

Funding

National Natural Science Foundation of China 82070041
6 · The paper itself

Abstract

backgroundChronic obstructive pulmonary disease (COPD) is a progressive disease characterized by chronic airway inflammation and remodeling. Fibrinogen gamma chain (FGG) has been implicated in the pathogenesis of multiple inflammatory and fibrotic conditions. However, the role and mechanisms of FGG in COPD remain unclear.

methodsFGG expression in lung tissues and plasma of COPD patients and CS-exposed mice was assessed. To investigate its functional role in cigarette smoke extract (CSE)-induced inflammation and epithelial-mesenchymal transition (EMT), we employed FGG knockdown (KD) and recombinant human FGG (rFGG) protein treatment in BEAS-2B cells and in a murine COPD model. To elucidate the related mechanisms in CSE-induced airway inflammation and EMT, BEAS-2B cells were treated with PF573228 (10 µM, a FAK inhibitor) or SB431542 (10 µM, a TGF-β type I receptor inhibitor).

resultsFGG was up-regulated in both the lung tissue and plasma of COPD patients. Plasma FGG levels were negatively correlated with lung function in COPD patients. Similarly, elevated FGG expression was verified in CS-exposed mice and CSE-induced BEAS-2B cells. Both in vitro (FGG-KD in BEAS-2B) and in vivo (mouse model) experiments demonstrated that inhibition of FGG expression attenuated CSE-induced inflammatory cytokine release and EMT. Treatment with PF573228 or SB431542 inhibited airway inflammation and EMT, implicating the focal adhesion and TGF-β/Smad2 pathways.

conclusionsFGG contributes to airway inflammation and remodeling in COPD. Cigarette smoke enhances FGG expression and secretion in bronchial epithelium. Increased FGG promotes the release of inflammatory cytokines and EMT through the focal adhesion and TGF-β/Smad2 pathways.

Indexed as

Airway RemodelingFibrinogenLungPneumoniaPulmonary Disease, Chronic ObstructiveSmad2 ProteinTransforming Growth Factor betaAgedAnimalsCell LineDisease Models, AnimalEpithelial-Mesenchymal TransitionFemaleHumansMaleMiceFibrinogenSmad2 ProteinSMAD2 protein, humanSmad2 protein, mouseSmokeTransforming Growth Factor betaAirway epithelium inflammationChronic obstructive pulmonary diseaseEpithelial-mesenchymal transitionFibrinogen gamma chain

Identifiers

PMID41254304

What OpenQuestion 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 OpenQuestion graph.