ArticleFrontiers in pharmacology2021
Iron-Dependent Mitochondrial Dysfunction Contributes to the Pathogenesis of Pulmonary Fibrosis.
Article in Frontiers in pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 49 citations in OpenAlex.
- Engineered exosomes encapsulated miR-218-5p alleviate the progression of PMRedox biology · 2026Article
- Advances in metabolic reprogramming of pulmonary fibrosis.Chinese medical journal pulmonary and critical care medicine · 2026Review
- Exploring Ferroptosis: A Key Mechanism in Respiratory System Diseases and its Therapeutic Potential.Applied biochemistry and biotechnology · 2026Review
- Regulated Cell Death in Idiopathic Pulmonary Fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- Next-Generation In Vitro Pulmonary Platforms for Respiratory Disease Modelling and Therapeutic Development: Current Advances and Future Prospects.Medicina (Kaunas, Lithuania) · 2026Review
- Targeting ATP11B-YAP axis repairs mitochondrial function and inhibits neuronal ferroptosis to attenuate age-related cognitive decline.Signal transduction and targeted therapy · 2026Article
- The interplay of ferroptosis and oxidative stress in pulmonary fibrosis: from mechanisms to treatment.Frontiers in cell and developmental biology · 2026Review
- A novel strategy for the protective effect of ginsenoside Rg1 against ovarian reserve decline by the PINK1 pathway.Pharmaceutical biology · 2025Article
- Iron metabolism dysregulation and ferroptosis: Emerging drivers in pulmonary fibrosis pathogenesis and therapy.Molecules and cells · 2025Review
- Iron metabolism in rheumatic diseases.Journal of translational autoimmunity · 2025Review
- The Causal Effect of Iron Traits on Risk of Hypertrophic Scarring: A Two-Sample Mendelian Randomization Study.Journal of cosmetic dermatology · 2025Article
- Ferroptosis: the potential key roles in idiopathic pulmonary fibrosis.European journal of medical research · 2025Review
- OC-STAMP is a potential biomarker and therapeutic target for Silicosis: an exploratory investigation.Journal of translational medicine · 2025Article
- The molecular and metabolic landscape of ferroptosis in respiratory diseases: Pharmacological aspects.Journal of pharmaceutical analysis · 2025Review
- Association of dietary iron intake with diabetic kidney disease among individuals with diabetes.Endocrine · 2024Article
- Emerging roles of ferroptosis in pulmonary fibrosis: current perspectives, opportunities and challenges.Cell death discovery · 2024Review
- Exploratory Analysis of Image-Guided Ionizing Radiation Delivery to Induce Long-Term Iron Accumulation and Ferritin Expression in a Lung Injury Model: Preliminary Results.Bioengineering (Basel, Switzerland) · 2024Article
- Ferroptosis in organ fibrosis: From mechanisms to therapeutic medicines.Journal of translational internal medicine · 2024Article
- SB431542 partially inhibits high glucose-induced EMT by restoring mitochondrial homeostasis in RPE cells.Cell communication and signaling : CCS · 2024Article
- Multiple roles of mitochondrial autophagy receptor FUNDC1 in mitochondrial events and kidney disease.Frontiers in cell and developmental biology · 2024Review
Corrections and comments
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Authors and funding
15 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although the pathogenesis of pulmonary fibrosis remains unclear, it is known to involve epithelial injury and epithelial-mesenchymal transformation (EMT) as a consequence of cigarette smoke (CS) exposure. Moreover, smoking deposits iron in the mitochondria of alveolar epithelial cells. Iron overload in mitochondria causes the Fenton reaction, leading to reactive oxygen species (ROS) production, and ROS leakage from the mitochondria induces cell injury and inflammation in the lungs. Nevertheless, the mechanisms underlying iron metabolism and pulmonary fibrosis are yet to be elucidated. In this study, we aimed to determine whether iron metabolism and mitochondrial dysfunction are involved in the pathogenesis of pulmonary fibrosis. We demonstrated that administration of the iron chelator deferoxamine (DFO) reduced CS-induced pulmonary epithelial cell death, mitochondrial ROS production, and mitochondrial DNA release. Notably, CS-induced cell death was reduced by the administration of an inhibitor targeting ferroptosis, a unique iron-dependent form of non-apoptotic cell death. Transforming growth factor-β-induced EMT of pulmonary epithelial cells was also reduced by DFO. The preservation of mitochondrial function reduced Transforming growth factor-β-induced EMT. Furthermore, transbronchial iron chelation ameliorated bleomycin-induced pulmonary fibrosis and leukocyte migration in a murine model. Our findings indicate that iron metabolism and mitochondrial dysfunction are involved in the pathogenesis of pulmonary fibrosis. Thus, they may be leveraged as new therapeutic targets for pulmonary fibrosis.
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