摘要
铜是人体必需微量元素,但过量会引发细胞凋亡,心脏作为氧化应激敏感器官,心肌细胞内铜超载会造成严重损害。细胞内铜稳态依赖吸收、利用和输出等环节,铜伴侣参与铜的细胞内运输与利用,细胞质有抵御铜超载的内源性防线。线粒体是活性氧(ROS)主要来源,也有防御ROS机制。缺氧时,心肌细胞铜超载使ROS生成增加,形成“缺氧-铜蓄积-氧化应激”恶性循环。此外,铜超载通过影响氧供需、介导ROS致心肌缺血-再灌注损伤、损害心肌兴奋-收缩耦联等造成心肌损伤。本文通过分析细胞铜代谢、ROS的产生与清除机制,旨在探讨细胞铜超载如何介导ROS的生成,进而引起心脏停搏后心肌损伤,为供心保护提供理论依据和新思路。
Copper is an essential trace element,but its overload triggers cellular apoptosis.The heart,being highly sensitive to oxidative stress,suffers severe damage under myocardial copper overload.While intracellular copper homeostasis is maintained by absorption,utilization,and export mechanisms mediated by copper chaperones,endogenous defense against copper overload exist in the cytosol..Mitochondria,the primary source of reactive oxygen species(ROS),possess intrinsic antioxidant systems.During hypoxia,copper accumulation in cardiomyocytes exacerbates ROS generation,establishing a pathological cycle of“hypoxia-copper accumulation-oxidative stress”.Crucially,copper overload induces post-arrest myocardial injury through three interconnected pathways:disruption of cardiac oxygen supply-demand balance;aggravation of ROS-mediated ischemia-reperfusion injury;and impairment of excitation-contraction coupling.This paper analyzes the mechanisms of cellular copper metabolism and the generation and scavenging of ROS.It aims to explore how cellular copper overload mediates ROS generation and subsequently causes myocardial injury after cardiac arrest,providing a theoretical basis and new ideas for donor heart protection.
作者
崔晨艺
李钊希
程兆云
钱晓亮
Cui Chenyi;Li Zhaoxi;Cheng Zhaoyun;Qian Xiaoliang(Department of Cardiac Surgery,Central China Fuwai Hospital of Zhengzhou University,Henan Zhengzhou 451464,China;Henan Provincial Clinical Medical Research Center for Cardiovascular Diseases,Henan Zhengzhou 451464,China)
出处
《中国体外循环杂志》
2025年第4期373-378,共6页
Chinese Journal of Extracorporeal Circulation
基金
河南省医学科技攻关计划项目(SBG202101005)。
关键词
铜超载
线粒体
活性氧
心肌损伤
心肌保护
Copper overload
Mitochondrion
Reactive oxygen species
Myocardial injury
Myocardial protection
