Molecular mechanism of MEF2C in ferroptosis-related asthma based on bioinformatics
10.12007/j.issn.0258-4646.2025.03.002
- VernacularTitle:基于生物信息学探讨MEF2C在铁死亡相关哮喘中的分子机制
- Author:
Haisong JIANG
1
;
Yilan SONG
1
Author Information
1. 延边大学医学院解剖学教研室,吉林省过敏性常见疾病免疫与靶向研究重点实验室,吉林 延吉 133002
- Publication Type:Journal Article
- Keywords:
asthma;
ferroptosis;
bioinformatics;
MEF2C;
interlukin-17A
- From:
Journal of China Medical University
2025;54(3):199-203
- CountryChina
- Language:Chinese
-
Abstract:
Objective Key genes related to ferroptosis in asthma were screened using bioinformatics,and their molecular mechanisms of action in the development of asthma were investigated.Methods Data sets related to asthma were obtained from the GEO database,and ferroptosis-related genes in FerrDB were downloaded to screen differentially expressed genes related to ferroptosis in asthma.LASSO regression and SVM-RFE algorithm were used to further screen the core genes.Molecular biology verification of these screened genes was performed,and miRNA microarray data from asthmatic mice combined with miRWalk and TargetScan were used to predict the upstream miRNA.Results From GSE43696,212 differentially expressed genes with consistent phenotypes in moderate-to-severe asthma were screened,including five ferroptosis-related genes:HCAR1,NOS2,MEF2C,IL6 and NOX1.The SVM-RFE results indicate that MEF2C has the greatest impact on the model.Experimental validation showed that the expression of both its mRNA and protein products was downregulated in asthmatic mice and was primarily expressed in the airway epithelium as well as within the cell nucleus.The prediction analysis results of miRNA targeting MEF2C revealed that miR-2861,which is upregulated in asthmatic mice,may target MEF2C,and that the expression of miR-2861 was significantly downregulated after IL-17A knockout.Conclusion MEF2C is a key regulator in ferropto-sis-related asthma.Its down regulation may be associated with IL-17A-mediated upregulation of miR-2861.
