Comprehensive bioinformatics analysis of the common mechanism of atherosclerosis and atrial fibrillation: emphasizing mitochondrial metabolic disorder and immune inflammation

This study establishes MRPS23 as a novel biomarker bridging mitochondrial dysfunction and immune dysregulation in AS and AF comorbidity. Its decline in AS suggests a potential role in mitochondrial ribosomal integrity loss driving metabolic stress, while immune-microenvironment interactions highlight its pleiotropic impacts on inflammatory cascades. These findings advance the "mitochondria-immune axis" paradigm for cardiovascular comorbidity, offering MRPS23 as a dual-disease therapeutic target. Further validation in preclinical models and clinical cohorts is needed to translate these insights into diagnostic or therapeutic applications.