Cardiovascular diseases remain a leading cause of mortality worldwide. Despite significant advances in diagnosis and treatment，elucidating novel mechanisms underlying their pathogenesis is still pivotal. Copper，an essential trace element for life activities，plays a critical role in maintaining cardiac myocyte energy supply and normal function，relying on finely regulated homeostasis within the body，particularly inside mitochondria. However，disruption of copper homeostasis can induce myocardial injury through multiple mechanisms. Excess copper can specifically trigger a copper - dependent mitochondrial response by binding to lipoylated enzymes in the tricarboxylic acid cycle，leading to iron-sulfur（Fe-S）cluster deficiency，protein aggregation，and prototoxic stress，ultimately resulting in cuproptosis. This review aims to summarize the molecular mechanisms of copper homeostasis and cuproptosis，as well as their recent research progress in cardiovascular diseases，hoping to provide a theoretical basis for precise prevention and treatment of these conditions.