Abstract
Atherosclerosis (AS) is a chronic inflammatory disease associated with lipid deposition in the vascular intima. Copper is a vital trace element implicated in the onset and progression of AS. Excessive intracellular copper accumulation induces a unique form of cell death termed "cuproptosis." The emergence of the concept of cuproptosis has highlighted the potential role of copper in AS. This review explores the regulatory mechanisms of copper metabolism and cuproptosis, summarizes recent findings on the link between copper excess and AS, and examines how cuproptosis may influence AS progression. The goal is to propose novel diagnostic and therapeutic strategies for AS through the lens of cuproptosis.