ArticleInternational journal of chronic obstructive pulmonary disease2023
Relationship Between ACSL4-Mediated Ferroptosis and Chronic Obstructive Pulmonary Disease.
Article in International journal of chronic obstructive pulmonary disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- Breaking the cycle of fibrosis: Ferroptosis as a therapeutic target (Review).International journal of molecular medicine · 2026Review
- Ferroptosis in e-cigarette aerosol-associated respiratory injury.Archives of toxicology · 2026Review
- Cystatin C prevents tissue injury after lung transplantation.Life science alliance · 2026Article
- Ironing out COPD: ferroptosis-driven immune dysregulation, metabolic rewiring, and precision therapeutic opportunities.Frontiers in immunology · 2026Review
- Prognostic Relevance of ACSL4 as a Serological Marker and Its Mediating Roles in Acute Supratentorial Intracerebral Hemorrhage: An Observational Analytical Study.International journal of general medicine · 2026Article
- Ferroptosis in smoke inhalation injury: from mechanisms to potential therapeutic targets.Frontiers in cell and developmental biology · 2026Review
- Mitochondrial dysfunction and the regulatory cell death crosstalk network in chronic obstructive pulmonary disease: from oxidative stress mechanisms to targeted therapeutic strategies.Frontiers in immunology · 2026Review
- Identification of ferroptosis-related genes involved in chronic obstructive pulmonary disease based on bioinformatics analysis.Animal models and experimental medicine · 2025Article
- Review
- Associations between serum levels of ferroptosis-related molecules and outcomes in stable COPD: an exploratory prospective observational study.Internal and emergency medicine · 2025Observational
- CircRNA_1156 Attenuates Neodymium Nitrate-Induced Hepatocyte Ferroptosis by Inhibiting the ACSL4/PKCβII Signaling Pathway.Antioxidants (Basel, Switzerland) · 2025Article
- Fluorofenidone alleviates cigarette smoke exposure-induced chronic lung injury by targeting ferroptosis.Scientific reports · 2024Article
- Integrated network pharmacology and transcriptomics to explore the mechanism of compound Dihuang granule (CDG) protects dopaminergic neurons by regulating the Nrf2/HMOX1 pathway in the 6-OHDA/MPPChinese medicine · 2024Article
- Mechanisms and therapeutic targets of ferroptosis: Implications for nanomedicine design.Journal of pharmaceutical analysis · 2024Review
- Silencing KLF6 Alleviates Cigarette Smoke Extract-Induced Mitochondrial Dysfunction in Bronchial Epithelial Cells by SIRT4 Upregulation.International journal of chronic obstructive pulmonary disease · 2024Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Although cigarette smoke exposure is the major risk factor for chronic obstructive pulmonary disease (COPD), the mechanism is not completely understood. The aim of the present study was to investigate whether ACSL4-mediated ferroptosis in lung epithelial cells plays a part in the COPD development process and its association. Patients and Methods: In this study, animal and cell models of COPD were modelled using cigarette smoke extracts (CSEs), and cell viability, lipid ROS, iron ion deposition, and ferroptosis-related markers were measured in lung tissue and lung epithelial cells following CSE exposure. Morphological changes in mitochondria were observed in lung tissue and epithelial cells of the lung by transmission electron microscope. The expression levels of ACSL4 mRNA and protein in lung tissue and epithelial cells were measured by real-time PCR and Western blotting. In addition, animal-interfering lentivirus and cell-interfering RNA against ACSL4 were constructed in this study, ferroptosis in lung tissue and lung epithelial cells after ACSL4 interference was detected, and ACSL4 mRNA and protein expression levels were detected. Results: CSE induced ferroptosis in lung tissues and lung epithelial cells, and the expression levels of ACSL4 were elevated in CSE-treated lung tissues and lung epithelial cells. After ACSL4 interference, the expression of ACSL4 decreased, mitochondrial morphology was restored, and ferroptosis in lung tissues and lung epithelial cells was alleviated. Both respiratory frequency and enhanced pause of COPD mice models decreased after ACSL4 interference. Conclusion: ACSL4-mediated ferroptosis in lung epithelial cells is associated with COPD and positively correlated with ferroptosis in epithelial cells.
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