Copper, an essential trace element in the human body, is pivotal in numerous physiological functions, including mitochondrial respiration, antioxidant reactions, and the synthesis of biological macromolecules. The cellular copper content is tightly regulated, as both copper deficiency and copper overload can be detrimental and lead to the onset of various diseases. Recently, a novel form of cell death known as Cuproptosis has been identified, which is triggered by an excess of copper. Excessive intracellular copper promotes the degradation of Fe-S cluster proteins and protein toxicity by stimulating the sulfur-acylation aggregation process of mitochondria-related proteins, ultimately resulting in cell death. With the emergence of the concept of copper-induced cell death, researchers have shifted their focus towards understanding the potential role of copper in atherosclerosis. This review delves into the regulatory mechanisms of copper metabolism and cuproptosis, encapsulates current research connecting an abundance of copper to atherosclerosis, and examines how cuproptosis influences atherosclerosis progression, with the goal of devising novel approaches for atherosclerosis prevention and management through cuproptosis.