Copper homeostasis and copper-induced cell death in the pathogenesis of cardiovascular disease and therapeutic strategies

Copper is a vital mineral, and an optimal amount of copper is required to support normal physiologic processes in various systems, including the cardiovascular system. Over the past few decades, copper-induced cell death, named cuproptosis, has become increasingly recognized as an important process mediating the pathogenesis and progression of cardiovascular disease (CVD), including atherosclerosis, stroke, ischemia-reperfusion injury, and heart failure. Therefore, an in-depth understanding of the regulatory mechanisms of cuproptosis in CVD may be useful for improving CVD management. Here, we review the relationship between copper homeostasis and cuproptosis-related pathways in CVD, as well as therapeutic strategies addressing copper-induced cell death in CVD.

Automated summary

Copper is a vital mineral for normal physiological processes, including cardiovascular systems. However, copper-induced cell death has been recognized as an important factor in the pathogenesis and progression of cardiovascular disease. Understanding the mechanisms of copper-induced cell death can help improve cardiovascular disease management. This review explores the relationship between copper homeostasis and pathways related to copper-induced cell death in cardiovascular disease, as well as therapeutic strategies.