Atherosclerosis is a complex systemic inflammatory metabolic disease, which originates from endothelial dysfunction and progresses through plaque formation involving vascular smooth muscle cells (VSMCs) and macrophage uptake of modified low-density lipoprotein (LDL). These processes lead to vascular stenosis, plaque rupture, and potentially sudden death. Metabolic dysregulation and cellular remodeling are fundamental to the pathogenesis of atherosclerosis. In this review, we summarize recent advances in the metabolic reprogramming of major cell types (including endothelial cells, VSMCs, and macrophages) during atherosclerosis progression. Furthermore, we discuss the crosstalk among these cells mediated by such metabolic alterations. Finally, we highlight the implications of metabolic reprogramming for targeted therapeutic strategies, offering insights for precision intervention in aortic atherosclerosis.
Liu et al. (Sun,) studied this question.