Work

Integrative analysis of genes provides insights into the molecular and immune characteristics of mitochondria-related genes in atherosclerosis

Year: 2025

Type: article

Abstract: Atherosclerosis is a chronic inflammatory disease characterized by lipid accumulation in arterial walls. The role of the interplay between mitochondrial dysfunction and immune inflammation in atherosclerosis is still unclear. This study aimed to investigate the molecular characteristics and immune landscape of mitochondrial hub genes involved in atherosclerosis. Based on bioinformatics analysis, three hub Mitochondria-related DEGs (MitoDEGs), including OXCT1, UCP2, and CPT1B, were screened out and showed good diagnostic performance in identifying atherosclerosis patients and controls. Immune analysis demonstrated strong correlations between hub MitoDEGs and immune cells, such as macrophages and T cells. Additionally, the predicted transcription factors of these hub MitoDEGs were significantly enriched in Th17, Th1 and Th2 cell differentiation signaling pathways. Both cell and animal experiments confirmed the expression trends of OXCT1 and CPT1B observed in the bioinformatics analysis. These hub MitoDEGs may play an important role in coordinating mitochondrial metabolism in the immune inflammation of atherosclerosis. • Mitochondrial-Immune Interplay in Atherosclerosis: This study uncovers the significant relationship between mitochondrial dysfunction and immune inflammation in atherosclerosis, highlighting the need for further investigation. • Key Mitochondrial-Related Genes Identified: Comprehensive bioinformatics analysis reveals hub mitochondrial-related differentially expressed genes, such as OXCT1, UCP2, and CPT1B, which may coordinate mitochondrial metabolism and immune responses. • Diagnostic and Therapeutic Insights: The research assesses the diagnostic potential of identified hub mitochondrial genes using ROC analysis and validates findings through cell and animal experiments, suggesting new diagnostic and therapeutic targets.

Source: Genomics

DOI: 10.1016/j.ygeno.2025.111013