Deciphering the Role of Copper Homeostasis in Atherosclerosis: From Molecular Mechanisms to Therapeutic Targets

Cardiovascular disease (CVD) is a leading cause of death globally, with atherosclerosis (AS) playing a central role in its pathogenesis as a chronic inflammatory condition. Copper, an essential trace element in the human body, participates in various biological processes and plays a significant role in the cardiovascular system. Maintaining normal copper homeostasis is crucial for cardiovascular health, and dysregulation of copper balance is closely associated with the development of CVD. When copper homeostasis is disrupted, it can induce cell death, which has been proposed to be a novel form of "cuproptosis", distinct from traditional programmed cell death. This new form of cell death is closely linked to the occurrence and progression of AS. This article elaborately describes the physiological mechanisms of copper homeostasis and explores its interactions with signaling pathways related to AS. Additionally, we focus on the process and mechanism of cell death induced by imbalances in copper homeostasis and summarize the relationship between copper homeostasis-related genes and AS. We also emphasize potential therapeutic approaches, such as copper balance regulators and nanotechnology interventions, to adjust copper levels in the body, providing new ideas and strategies for the prevention and treatment of CVD.