Cross-disease metabolic reprogramming: bridging atherosclerosis and cancer for therapy

Atherosclerosis and cancer have traditionally been regarded as distinct disease categories; however, recent research has identified numerous metabolic commonalities between them. Both conditions involve immune cells, endothelial cells, and vascular smooth muscle cells within their respective microenvironments, with the addition of tumor cells in cancer. These cellular components exhibit metabolic profiles that are analogous, albeit not identical. Such characteristics include enhanced glycolysis, increased activity of the pentose phosphate pathway, dysregulated lipid and cholesterol metabolism, altered amino acid utilization, and reprogrammed mitochondrial energy metabolism. These metabolic alterations not only fulfill the survival and proliferation requirements of cells in high-stress environments but also contribute significantly to key pathological processes, including the regulation of inflammation, immune evasion, and tissue remodeling. Using metabolic reprogramming pathways and mechanisms as a foundational framework, this review systematically compares the interconnections between atherosclerosis and cancer. It elucidates the intrinsic relationship between cellular fate transitions and disease progression, aiming to provide a theoretical foundation for the exploration of potential common therapeutic targets and cross-disease treatment strategies.