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Published on: January 16, 2013
Analysis of m7G methylation modification patterns and pulmonary vascular immune microenvironment in pulmonary
Desheng Wang1, Yanfei Mo1, Dongfang Zhang2
1Department of Clinical Pharmacology, School of Pharmacy, China Medical University, Shenyang, Liaoning, China.
Background:
M7G methylation modification plays an important role in cardiovascular disease development. Dysregulation of the immune microenvironment is closely related to the pathogenesis of PAH. However, it is unclear whether m7G methylation is involved in the progress of PAH by affecting the immune microenvironment.
Methods:
The gene expression profile of PAH was obtained from the GEO database, and the m7G regulatory factors were analyzed for differences. Machine learning algorithms were used to screen characteristic genes, including the least absolute shrinkage and selection operator, random forest, and support vector machine recursive feature elimination analysis. Constructed a nomogram model, and receiver operating characteristic was used to evaluate the diagnosis of disease characteristic genes value. Next, we used an unsupervised clustering method to perform consistent clustering analysis on m7G differential genes. Used the ssGSEA algorithm to estimate the relationship between the m7G regulator in PAH and immune cell infiltration and analyze the correlation with disease-characteristic genes. Finally, the listed drugs were evaluated through the screened signature genes.
Results:
We identified 15 kinds of m7G differential genes. CYFIP1, EIF4E, and IFIT5 were identified as signature genes by the machine learning algorithm. Meanwhile, two m7G molecular subtypes were identified by consensus clustering (cluster A/B). In addition, immune cell infiltration analysis showed that activated CD4 T cells, regulatory T cells, and type 2 T helper cells were upregulated in m7G cluster B, CD56 dim natural killer cells, MDSC, and monocyte were upregulated in the m7G cluster A. It might be helpful to select Calpain inhibitor I and Everolimus for the treatment of PAH.
Conclusion:
Our study identified CYFIP1, EIF4E, and IFIT5 as novel diagnostic biomarkers in PAH. Furthermore, their association with immune cell infiltration may facilitate the development of immune therapy in PAH.
Insights
This study reveals that m7G methylation regulators, specifically CYFIP1, EIF4E, and IFIT5, are linked to pulmonary arterial hypertension (PAH) and immune cell infiltration, offering potential diagnostic biomarkers and therapeutic targets for PAH.
Area of Science:
- Cardiovascular Research
- Immunology
- Molecular Biology
Background:
- M7G methylation is implicated in cardiovascular disease.
- Immune microenvironment dysregulation is key in pulmonary arterial hypertension (PAH) pathogenesis.
- The role of m7G methylation in PAH via immune modulation remains unclear.
Purpose of the Study:
- To investigate the involvement of m7G methylation regulators in PAH.
- To identify potential diagnostic biomarkers for PAH.
- To explore the relationship between m7G methylation and immune cell infiltration in PAH.
Main Methods:
- Utilized gene expression data from the GEO database for PAH.
- Employed machine learning algorithms (LASSO, Random Forest, SVM-RFE) to screen characteristic m7G regulatory factors.
- Performed consensus clustering to identify m7G molecular subtypes and ssGSEA to analyze immune cell infiltration.
Main Results:
- Identified 15 m7G differential genes, with CYFIP1, EIF4E, and IFIT5 selected as signature genes.
- Discovered two m7G molecular subtypes (cluster A/B) associated with distinct immune cell infiltration patterns.
- Upregulation of specific immune cells (T cells, NK cells, MDSC, monocytes) observed in different clusters.
Conclusions:
- CYFIP1, EIF4E, and IFIT5 are novel diagnostic biomarkers for PAH.
- The identified m7G regulators and their association with immune infiltration may guide the development of immune therapies for PAH.
