Copper homeostasis and cardiovascular disease: molecular mechanisms and pathophysiological role

Cardiovascular disease is the main cause of human death worldwide and its incidence rate and mortality are increasing year by year. Effective intervention and management measures are urgently needed to improve the prognosis of patients. Although previous studies have explored the pathogenesis of cardiovascular disease, its specific molecular mechanisms have not been fully elucidated. Copper ions are one of the most important signaling molecules in cells and their dynamic balance is involved in various biological processes such as oxidative stress, energy metabolism and signal transmission in the human body. Copper deficiency or overload can lead to the occurrence and development of adverse cardiovascular events. Recent studies have shown that cuproptosis is a new type of programmed cell death that is different from cell apoptosis, necroptosis, pyroptosis, autophagy and ferroptosis, and it is involved and plays an important role in cardiac remodeling, atherosclerosis, coronary heart disease, cardiomyopathy, arrhythmia, heart failure and other cardiovascular pathophysiological processes and disease development. This article summarizes the molecular mechanisms and pathophysiological roles of copper homeostasis and cuproptosis in cardiovascular diseases, which is expected to provide new targets or strategies for the diagnosis, treatment and prognosis of cardiovascular diseases.