铜死亡机制及其在动脉粥样硬化中的研究进展

The Mechanism of Cuproptosis and Its Advancements in Atherosclerosis Research

铜是人体内必需的微量元素,在线粒体呼吸、抗氧化反应、生物大分子合成等多种生理过程中发挥着至关重要的作用。在细胞内,铜的含量受到严格调节,因为铜缺乏和铜过量都是有害的,并可能导致各种疾病的发生。铜死亡是一种新近报道的由过量铜引起的新型细胞死亡形式。胞内铜的作用会刺激线粒体相关蛋白的硫辛酰化并导致其聚集,进而引发铁硫蛋白的降解和蛋白毒性反应,最终造成细胞死亡。随着铜诱导细胞死亡概念的出现,研究人员开始关注铜在动脉粥样硬化(As)中的潜在作用。本文综述了铜代谢和铜死亡的调节机制,总结了铜过量与As之间联系的现有研究,并对铜死亡影响As发展的机制进行讨论,旨在从铜死亡的角度为As的防治提供新的策略。

Copper,an essential trace element in the human body,is pivotal in numerous physiological functions,including mitochondrial respiration,antioxidant reactions,and the synthesis of biological macromolecules.The cellular copper content is tightly regulated,as both copper deficiency and copper overload can be detrimental and lead to the onset of various diseases.Recently,a novel form of cell death known as Cuproptosis has been identified,which is triggered by an excess of copper.Excessive intracellular copper promotes the degradation of Fe-S cluster proteins and protein toxicity by stimulating the sulfur-acylation aggregation process of mitochondria-related proteins,ultimately resulting in cell death.With the emergence of the concept of copper-induced cell death,researchers have shifted their focus towards understanding the potential role of copper in atherosclerosis.This review delves into the regulatory mechanisms of copper metabolism and cuproptosis,encapsulates current research connecting an abundance of copper to atherosclerosis,and examines how cuproptosis influences atherosclerosis progression,with the goal of devising novel approaches for atherosclerosis prevention and management through cuproptosis.