This graphic depicts the interplay between copper homeostasis and cuproptosis and their role in cardiovascular diseases. Copper is vital for cardiac mitochondrial function, while its dysregulation induces cuproptosis via Ferredoxin1 (FDX1) and lipoic acid synthase (LIAS). Cuproptosis is linked to myocardial ischemia/reperfusion injury, heart failure, atherosclerosis, and arrhythmias. Copper deficiency impacts atherosclerosis markers. Therapeutic interventions include copper chelators (e.g., ammonium tetrathiomolybdate), and oxidative phosphorylation inhibitors like elesclomol and copper ionophores (CuII(atsm), CuII(gtsm), and disulfiram). These interventions modulate intracellular copper, elevate NO, and reduce inflammatory cytokines, contributing to decreased cardiovascular diseases.

该图描绘了铜稳态和铜凋亡之间的相互作用及其在心血管疾病中的作用。铜对于心脏线粒体功能至关重要，而铜的失调会通过铁氧还蛋白 1 (FDX1) 和硫辛酸合酶 (LIAS) 诱导铜凋亡。铜中毒与心肌缺血/再灌注损伤、心力衰竭、动脉粥样硬化和心律失常有关。铜缺乏会影响动脉粥样硬化标志物。治疗干预措施包括铜螯合剂（例如四硫代钼酸铵）和氧化磷酸化抑制剂，如艾司氯醇和铜离子载体（CuII(atsm)、CuII(gtsm) 和双硫仑）。这些干预措施可调节细胞内铜、升高一氧化氮并减少炎症细胞因子，从而有助于减少心血管疾病。