Evidence map›Paper›PMID 40986113›Full record

ArticleLung2025

The Down-Regulation of Lactoferrin Expression Induced by Cigarette Smoke can Induce Ferroptosis in COPD.

Yuxiu Wang, Wenjing Xu, Kaiqi Ren, Jingjing Yang, Lingfeng Min

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Article in Lung, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

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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

2 citing papers in PubMed.

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4 · The record

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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

5 authors.

Yuxiu Wang *Department of Respiratory and Critical Care Medicine, Northern Jiangsu People's Hospital Affiliated to Yangzhou University, Yangzhou, 225001, Jiangsu, China.
Wenjing Xu *Department of Respiratory and Critical Care Medicine, Northern Jiangsu People's Hospital Affiliated to Yangzhou University, Yangzhou, 225001, Jiangsu, China.
Kaiqi RenDepartment of Respiratory and Critical Care Medicine, Northern Jiangsu People's Hospital Affiliated to Yangzhou University, Yangzhou, 225001, Jiangsu, China.
Jingjing YangDepartment of Respiratory and Critical Care Medicine, Northern Jiangsu People's Hospital Affiliated to Yangzhou University, Yangzhou, 225001, Jiangsu, China.
Lingfeng MinDepartment of Respiratory and Critical Care Medicine, Northern Jiangsu People's Hospital Affiliated to Yangzhou University, Yangzhou, 225001, Jiangsu, China. minlingfeng@126.com.

Funding

The Foundation for High-level Talents during the 13th Five-year Plan Period of Yangzhou, China ZDRC201866The National Natural Science Foundation of China 81870033
6 · The paper itself

Abstract

purposeLactoferrin (LTF) plays a crucial role in iron homeostasis, immune response, and inflammation. In the context of chronic obstructive pulmonary disease (COPD), LTF's expression is significantly influenced by environmental factors, particularly cigarette smoke. The pathological mechanism by which cigarette smoke regulates LTF and affects iron metabolism in COPD remains unclear. This study aims to clarify the mechanism therein.

methodsIn this study, cigarette smoke extract (CSE) was used to construct mouse and cell models of chronic obstructive pulmonary disease (COPD). Transcriptomic and proteomic tests were performed on the lung tissues of the mouse model of COPD to screen or measure the Hub gene. The interaction network prediction of LTF-related proteins was carried out using the STRING database. The Beas-2B cell model with LTF overexpression and interference was constructed by lentivirus transfection, and then the cell viability, cytotoxicity, lipid reactive oxygen species (ROS), iron ion deposition, and iron-related markers of bronchial epithelial cells after CSE exposure were detected. The morphological changes of mitochondria in bronchial epithelial cells were observed by transmission electron microscopy. The expression levels of ACSL4 and GPX4 proteins in bronchial epithelial cells were detected by Western blotting.

resultsThe expression of LTF is down-regulated in both lung tissue of the COPD mouse model and bronchial epithelial cells, and it plays a key role in ferroptosis of CSE-induced bronchial epithelial cells. In the LTF-interfered bronchial epithelial cells treated with CSE, ferroptosis-related markers (such as ROS and MDA) were significantly increased, GSH was significantly decreased, mitochondrial volume was reduced, cristae were decreased, the expression of ACSL4 protein was increased, while the expression of GPX4 protein was decreased. Meanwhile, overexpression of LTF can reverse the ferroptosis status of bronchial epithelial cells treated with CSE.

conclusionUnder CSE induction, the decrease in LTF expression level will lead to the accumulation of ferrous ions in bronchial epithelial cells and induce the occurrence of ferroptosis.

Indexed as

FerroptosisLactoferrinPulmonary Disease, Chronic ObstructiveSmokeAnimalsBronchiCell LineCoenzyme A LigasesDisease Models, AnimalDown-RegulationEpithelial CellsHumansIronLungMaleMiceCoenzyme A Ligasesglutathione peroxidase 4, mouseIronLactoferrinPhospholipid Hydroperoxide Glutathione PeroxidaseReactive Oxygen SpeciesSmokeChronic Obstructive Pulmonary Disease, COPDFerroptosisLactoferrin, LTF

Identifiers

PMID40986113

What Socratic holds

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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 Socratic graph.