Exploring cuproptosis as a mechanism and potential intervention target in cardiovascular diseases

Copper (Cu) is a vital trace element for maintaining human health. Current evidence suggests that genes responsible regulating copper influx and detoxification help preserve its homeostasis. Adequate Cu levels sustain normal cardiac blood vessel activity by mitochondrial function. Cuproptosis, unlike other forms of cell death, characterized alterations in enzymes. Therapeutics targeting cuproptosis cardiovascular diseases (CVDs) mainly include chelators, inhibitors chaperone proteins, ionophores. In this review, we expound on the primary mechanisms, critical signaling pathways involved cuproptosis, along with impact CVDs role it plays different types cells. Additionally, explored influence key regulatory proteins associated determined whether intervening metabolism can enhance outcomes CVDs. The insights from review provide fresh perspective pathogenesis new targets intervention these diseases.