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Utilizing Integrated Bioinformatics Analysis to Explore Potential Alterations in Mitochondrial Function Within Immune
Chang Guan1, Si-Xu Chen2, Chun-Ling Huang2
1Department of Cardiology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou 510120, China.
Bioengineering (Basel, Switzerland)
|February 26, 2025
Summary
Mitochondrial dysfunction in immune cells contributes to thoracic aortic aneurysm (TAA). This study identifies key genes and pathways involved in TAA pathogenesis, offering potential therapeutic targets.
Area of Science:
- Cardiovascular Biology
- Immunology
- Mitochondrial Biology
Background:
- Thoracic aortic aneurysm (TAA) is a serious vascular disease.
- Mitochondrial dysfunction in vascular cells is linked to TAA.
- The role of mitochondrial status in TAA immune cells is unclear.
Purpose of the Study:
- Investigate mitochondrial gene expression in TAA immune cells.
- Identify key mitochondrial genes and pathways in TAA.
- Explore the link between mitochondrial function and TAA pathogenesis.
Main Methods:
- Analyzed bulk and single-cell RNA sequencing data from TAA patients.
- Calculated a mitoscore to assess mitochondrial function.
- Used LASSO regression and SVM-RFE for gene identification and validated in mouse models.
Main Results:
- Identified differentially expressed mitochondrial-related genes (DE-MRGs) in TAA.
- Found mitochondrial-mediated apoptosis in M1 macrophages and fission in CD4+ T cells.
- Key genes (MUCB, ARRB2, FRG, ALPL) and methionine metabolism were linked to DE-MRGs.
Conclusions:
- Mitochondrial dysfunction is present in immune cells of TAA patients.
- Specific immune cell responses (apoptosis, fission) are mitochondrially driven.
- This research reveals novel insights into TAA pathogenesis and potential therapeutic avenues.
