CEACAM5 exacerbates asthma by inducing ferroptosis and autophagy in airway epithelial cells through the JAK/STAT6-dependent pathway
Objectives Asthma, a prevalent chronic disease, poses significant health threats and burdens healthcare systems. This study focused on the role of bronchial epithelial cells in asthma pathophysiology.Methods Bioinformatics was used to identify key asthmarelated genes. An ovalbumin-sensitized mouse m...
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Taylor & Francis Group
2025-12-01
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| Series: | Redox Report |
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| Online Access: | https://www.tandfonline.com/doi/10.1080/13510002.2024.2444755 |
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| author | Si Liu Li Chen Yunxiao Shang |
| author_facet | Si Liu Li Chen Yunxiao Shang |
| author_sort | Si Liu |
| collection | DOAJ |
| description | Objectives Asthma, a prevalent chronic disease, poses significant health threats and burdens healthcare systems. This study focused on the role of bronchial epithelial cells in asthma pathophysiology.Methods Bioinformatics was used to identify key asthmarelated genes. An ovalbumin-sensitized mouse model and an IL-13-stimulated Beas-2B cell model were established for further investigation.Results Carcinoembryonic antigen-related cell adhesion molecule 5 (CEACAM5) was identified as a crucial gene in asthma. CEACAM5 expression was elevated in asthmatic mouse lung tissues and IL-13-stimulated Beas-2B cells, primarily in bronchial epithelial cells. CEACAM5 induced reactive oxygen species (ROS), lipid peroxidation, and ferroptosis. Interfering with CEACAM5 reduced ROS, malondialdehyde levels, and enhanced antioxidant capacity, while inhibiting iron accumulation and autophagy. Overexpression of CEACAM5 in IL-13-stimulated cells activated the JAK/STAT6 pathway, which was necessary for CEACAM5-induced autophagy, ROS accumulation, lipid peroxidation, and ferroptosis.Conclusion CEACAM5 promotes ferroptosis and autophagy in airway epithelial cells via the JAK/STAT6 pathway, exacerbating asthma symptoms. It represents a potential target for clinical treatment. |
| format | Article |
| id | doaj-art-b4ba4b59811145b99411afae53308725 |
| institution | Kabale University |
| issn | 1351-0002 1743-2928 |
| language | English |
| publishDate | 2025-12-01 |
| publisher | Taylor & Francis Group |
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| series | Redox Report |
| spelling | doaj-art-b4ba4b59811145b99411afae533087252025-01-23T08:45:38ZengTaylor & Francis GroupRedox Report1351-00021743-29282025-12-0130110.1080/13510002.2024.2444755CEACAM5 exacerbates asthma by inducing ferroptosis and autophagy in airway epithelial cells through the JAK/STAT6-dependent pathwaySi Liu0Li Chen1Yunxiao Shang2Department of Pediatrics, Shengjing Hospital of China Medical University, Shenyang, People’s Republic of ChinaDepartment of Pediatrics, Shengjing Hospital of China Medical University, Shenyang, People’s Republic of ChinaDepartment of Pediatrics, Shengjing Hospital of China Medical University, Shenyang, People’s Republic of ChinaObjectives Asthma, a prevalent chronic disease, poses significant health threats and burdens healthcare systems. This study focused on the role of bronchial epithelial cells in asthma pathophysiology.Methods Bioinformatics was used to identify key asthmarelated genes. An ovalbumin-sensitized mouse model and an IL-13-stimulated Beas-2B cell model were established for further investigation.Results Carcinoembryonic antigen-related cell adhesion molecule 5 (CEACAM5) was identified as a crucial gene in asthma. CEACAM5 expression was elevated in asthmatic mouse lung tissues and IL-13-stimulated Beas-2B cells, primarily in bronchial epithelial cells. CEACAM5 induced reactive oxygen species (ROS), lipid peroxidation, and ferroptosis. Interfering with CEACAM5 reduced ROS, malondialdehyde levels, and enhanced antioxidant capacity, while inhibiting iron accumulation and autophagy. Overexpression of CEACAM5 in IL-13-stimulated cells activated the JAK/STAT6 pathway, which was necessary for CEACAM5-induced autophagy, ROS accumulation, lipid peroxidation, and ferroptosis.Conclusion CEACAM5 promotes ferroptosis and autophagy in airway epithelial cells via the JAK/STAT6 pathway, exacerbating asthma symptoms. It represents a potential target for clinical treatment.https://www.tandfonline.com/doi/10.1080/13510002.2024.2444755Bronchial epithelial cellsCEACAM5ferroptosisautophagyJAKSTAT6 |
| spellingShingle | Si Liu Li Chen Yunxiao Shang CEACAM5 exacerbates asthma by inducing ferroptosis and autophagy in airway epithelial cells through the JAK/STAT6-dependent pathway Redox Report Bronchial epithelial cells CEACAM5 ferroptosis autophagy JAK STAT6 |
| title | CEACAM5 exacerbates asthma by inducing ferroptosis and autophagy in airway epithelial cells through the JAK/STAT6-dependent pathway |
| title_full | CEACAM5 exacerbates asthma by inducing ferroptosis and autophagy in airway epithelial cells through the JAK/STAT6-dependent pathway |
| title_fullStr | CEACAM5 exacerbates asthma by inducing ferroptosis and autophagy in airway epithelial cells through the JAK/STAT6-dependent pathway |
| title_full_unstemmed | CEACAM5 exacerbates asthma by inducing ferroptosis and autophagy in airway epithelial cells through the JAK/STAT6-dependent pathway |
| title_short | CEACAM5 exacerbates asthma by inducing ferroptosis and autophagy in airway epithelial cells through the JAK/STAT6-dependent pathway |
| title_sort | ceacam5 exacerbates asthma by inducing ferroptosis and autophagy in airway epithelial cells through the jak stat6 dependent pathway |
| topic | Bronchial epithelial cells CEACAM5 ferroptosis autophagy JAK STAT6 |
| url | https://www.tandfonline.com/doi/10.1080/13510002.2024.2444755 |
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