MOLECULAR MECHANISMS LINKING INFLAMMATION AND CARDIOVASCULAR DISEASE

Abstract

Cardiovascular disease (CVD) remains a leading cause of global mortality, with atherosclerosis as its primary pathological basis. Increasing evidence suggests that inflammation plays a central role in the initiation and progression of atherosclerotic plaques. This study aimed to investigate the molecular mechanisms linking inflammation and cardiovascular disease using transcriptomic analysis of human carotid plaque samples. Gene expression profiles from early and advanced atherosclerotic lesions were analyzed to identify differentially expressed genes and associated biological pathways. The analysis revealed significant transcriptional differences between early and advanced plaques, with advanced lesions showing upregulation of genes involved in inflammatory signaling, immune activation, and extracellular matrix remodeling. Functional enrichment demonstrated that these genes were predominantly associated with cytokine-mediated signaling, leukocyte migration, and immune response pathways. Network analysis identified key regulatory genes with central roles in coordinating inflammatory processes. In addition, immune cell infiltration analysis indicated increased presence of inflammatory immune cells in advanced plaques, reflecting an active immune microenvironment. These findings suggest that progression of atherosclerosis is driven by coordinated activation of inflammatory pathways and immune responses. The integration of gene expression, pathway, and network analyses provides a comprehensive understanding of the molecular basis of inflammation in cardiovascular disease. The identified molecular signatures offer potential biomarkers and therapeutic targets for improved diagnosis and treatment.