Cellular copper overload mediates reactive oxygen species induced myocardial injury following cardiac arrest
Cui Chenyi
Li Zhaoxi
Cheng Zhaoyun
Qian Xiaoliang
Abstract：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.
Keywords：Copper overloadMitochondrionReactive oxygen speciesMyocardial injuryMyocardial protection
Publication Date：2025-08-28
Online Publishing Date：2025-08-27(First online date of this platform, not the publication date of the document)
Pages：6( 373-378 )