Ferroptosis: the potential key roles in idiopathic pulmonary fibrosis
Abstract Idiopathic pulmonary fibrosis (IPF) is a chronic progressive interstitial lung disease characterized by recurrent injury to alveolar epithelial cells, epithelial-mesenchymal transition, and fibroblast activation, which leads to excessive deposition of extracellular matrix (ECM) proteins. Ho...
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BMC
2025-04-01
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| Series: | European Journal of Medical Research |
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| Online Access: | https://doi.org/10.1186/s40001-025-02623-2 |
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| author | Longfei Song Fusheng Gao Jun Man |
| author_facet | Longfei Song Fusheng Gao Jun Man |
| author_sort | Longfei Song |
| collection | DOAJ |
| description | Abstract Idiopathic pulmonary fibrosis (IPF) is a chronic progressive interstitial lung disease characterized by recurrent injury to alveolar epithelial cells, epithelial-mesenchymal transition, and fibroblast activation, which leads to excessive deposition of extracellular matrix (ECM) proteins. However, effective preventative and therapeutic interventions are currently lacking. Ferroptosis, a unique form of iron-dependent lipid peroxidation-induced cell death, exhibits distinct morphological, physiological, and biochemical features compared to traditional programmed cell death. Recent studies have revealed a close relationship between iron homeostasis and the pathogenesis of pulmonary interstitial fibrosis. Ferroptosis exacerbates tissue damage and plays a crucial role in regulating tissue repair and the pathological processes involved. It leads to recurrent epithelial injury, where dysregulated epithelial cells undergo epithelial-mesenchymal transition via multiple signaling pathways, resulting in the excessive release of cytokines and growth factors. This dysregulated environment promotes the activation of pulmonary fibroblasts, ultimately culminating in pulmonary fibrosis. This review summarizes the latest advancements in ferroptosis research and its role in the pathogenesis and treatment of IPF, highlighting the significant potential of targeting ferroptosis for IPF management. Importantly, despite the rapid developments in this emerging research field, ferroptosis studies continue to face several challenges and issues. This review also aims to propose solutions to these challenges and discusses key concepts and pressing questions for the future exploration of ferroptosis. |
| format | Article |
| id | doaj-art-991ca426c7724075a91a67180612c044 |
| institution | Kabale University |
| issn | 2047-783X |
| language | English |
| publishDate | 2025-04-01 |
| publisher | BMC |
| record_format | Article |
| series | European Journal of Medical Research |
| spelling | doaj-art-991ca426c7724075a91a67180612c0442025-08-20T03:52:24ZengBMCEuropean Journal of Medical Research2047-783X2025-04-0130111610.1186/s40001-025-02623-2Ferroptosis: the potential key roles in idiopathic pulmonary fibrosisLongfei Song0Fusheng Gao1Jun Man2Department of Rehabilitation Medicine, Affiliated Hospital of Shandong Second Medical UniversityDepartment of Respiratory and Critical Care Medicine, Affiliated Hospital of Shandong Second Medical UniversityDepartment of Respiratory and Critical Care Medicine, Affiliated Hospital of Shandong Second Medical UniversityAbstract Idiopathic pulmonary fibrosis (IPF) is a chronic progressive interstitial lung disease characterized by recurrent injury to alveolar epithelial cells, epithelial-mesenchymal transition, and fibroblast activation, which leads to excessive deposition of extracellular matrix (ECM) proteins. However, effective preventative and therapeutic interventions are currently lacking. Ferroptosis, a unique form of iron-dependent lipid peroxidation-induced cell death, exhibits distinct morphological, physiological, and biochemical features compared to traditional programmed cell death. Recent studies have revealed a close relationship between iron homeostasis and the pathogenesis of pulmonary interstitial fibrosis. Ferroptosis exacerbates tissue damage and plays a crucial role in regulating tissue repair and the pathological processes involved. It leads to recurrent epithelial injury, where dysregulated epithelial cells undergo epithelial-mesenchymal transition via multiple signaling pathways, resulting in the excessive release of cytokines and growth factors. This dysregulated environment promotes the activation of pulmonary fibroblasts, ultimately culminating in pulmonary fibrosis. This review summarizes the latest advancements in ferroptosis research and its role in the pathogenesis and treatment of IPF, highlighting the significant potential of targeting ferroptosis for IPF management. Importantly, despite the rapid developments in this emerging research field, ferroptosis studies continue to face several challenges and issues. This review also aims to propose solutions to these challenges and discusses key concepts and pressing questions for the future exploration of ferroptosis.https://doi.org/10.1186/s40001-025-02623-2IPFFerroptosisEpithelial-mesenchymal transitionFibroblast activationTherapeutic targets |
| spellingShingle | Longfei Song Fusheng Gao Jun Man Ferroptosis: the potential key roles in idiopathic pulmonary fibrosis European Journal of Medical Research IPF Ferroptosis Epithelial-mesenchymal transition Fibroblast activation Therapeutic targets |
| title | Ferroptosis: the potential key roles in idiopathic pulmonary fibrosis |
| title_full | Ferroptosis: the potential key roles in idiopathic pulmonary fibrosis |
| title_fullStr | Ferroptosis: the potential key roles in idiopathic pulmonary fibrosis |
| title_full_unstemmed | Ferroptosis: the potential key roles in idiopathic pulmonary fibrosis |
| title_short | Ferroptosis: the potential key roles in idiopathic pulmonary fibrosis |
| title_sort | ferroptosis the potential key roles in idiopathic pulmonary fibrosis |
| topic | IPF Ferroptosis Epithelial-mesenchymal transition Fibroblast activation Therapeutic targets |
| url | https://doi.org/10.1186/s40001-025-02623-2 |
| work_keys_str_mv | AT longfeisong ferroptosisthepotentialkeyrolesinidiopathicpulmonaryfibrosis AT fushenggao ferroptosisthepotentialkeyrolesinidiopathicpulmonaryfibrosis AT junman ferroptosisthepotentialkeyrolesinidiopathicpulmonaryfibrosis |