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癌胚抗原相关细胞黏附分子5通过JAK/STAT6依赖性途径诱导气道上皮细胞发生铁死亡和自噬，从而加重哮喘。

CEACAM5 exacerbates asthma by inducing ferroptosis and autophagy in airway epithelial cells through the JAK/STAT6-dependent pathway.

作者信息

Liu Si, Chen Li, Shang Yunxiao

机构信息

Department of Pediatrics, Shengjing Hospital of China Medical University, Shenyang, People's Republic of China.

出版信息

Redox Rep. 2025 Dec;30(1):2444755. doi: 10.1080/13510002.2024.2444755. Epub 2025 Jan 23.

DOI:10.1080/13510002.2024.2444755
PMID:39844719
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11758806/
Abstract

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.

摘要

目的

哮喘是一种常见的慢性疾病，对健康构成重大威胁，并给医疗系统带来负担。本研究聚焦于支气管上皮细胞在哮喘病理生理学中的作用。

方法

运用生物信息学来识别关键的哮喘相关基因。建立卵清蛋白致敏小鼠模型和白细胞介素-13刺激的Beas-2B细胞模型用于进一步研究。

结果

癌胚抗原相关细胞黏附分子5（CEACAM5）被确定为哮喘中的关键基因。CEACAM5在哮喘小鼠肺组织和白细胞介素-13刺激的Beas-2B细胞中表达升高，主要在支气管上皮细胞中。CEACAM5诱导活性氧（ROS）、脂质过氧化和铁死亡。干扰CEACAM5可降低ROS、丙二醛水平，并增强抗氧化能力，同时抑制铁积累和自噬。在白细胞介素-13刺激的细胞中过表达CEACAM5激活了JAK/STAT6通路，这是CEACAM5诱导自噬、ROS积累、脂质过氧化和铁死亡所必需的。

结论

CEACAM5通过JAK/STAT6通路促进气道上皮细胞中的铁死亡和自噬，加剧哮喘症状。它代表了一个潜在的临床治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77e8/11758806/354c16d2f69e/YRER_A_2444755_F0007_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77e8/11758806/19e95f3e918a/YRER_A_2444755_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77e8/11758806/fb66124fbf8a/YRER_A_2444755_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77e8/11758806/bf1563661e92/YRER_A_2444755_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77e8/11758806/5d2479fd3ab9/YRER_A_2444755_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77e8/11758806/aa6a5fd7c9ba/YRER_A_2444755_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77e8/11758806/354c16d2f69e/YRER_A_2444755_F0007_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77e8/11758806/19e95f3e918a/YRER_A_2444755_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77e8/11758806/fb66124fbf8a/YRER_A_2444755_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77e8/11758806/bf1563661e92/YRER_A_2444755_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77e8/11758806/5d2479fd3ab9/YRER_A_2444755_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77e8/11758806/aa6a5fd7c9ba/YRER_A_2444755_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77e8/11758806/354c16d2f69e/YRER_A_2444755_F0007_OC.jpg

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