Atherosclerosis (As) is a chronic inflammatory disease associated with lipid deposition. Copper is considered to be an important trace element and is closely related to the occurrence and development of As. Excessive accumulation of copper ions in cells can induce cell death, a new type of cell death named “cuproptosis”. Under normal conditions, the body's copper metabolism can control the copper level in a stable range. When the disease occurs, copper homeostasis is destroyed, intracellular copper overload produces cytotoxicity, induces oxidative stress, inflammation, cell pyroptosis and cuproptosis, and promotes the occurrence and development of As. This article summarizes the relationship between copper levels and As, and discusses the mechanism of cuproptosis and the pathological mechanism of copper overload promoting As from the perspective of the body's copper regulation, and reviews the relevant drug intervention, expecting to provide a new therapeutic target for As.