硝基化修饰蛋白质在心血管内皮功能障碍中的作用

The role of nitrated modified proteins in cardiovascular endothelial dysfunction

内皮功能障碍作为多种心血管疾病共同的特征之一,与过量表达的活性氧(ROS)/活性氮(RNS)密切相关。超氧阴离子与一氧化氮(NO)反应可以生成氧化能力更强的过氧亚硝酸盐,可以通过氧化多种蛋白质耗竭NO,导致内皮收缩与舒张功能障碍,在多种心血管疾病中发挥了重要的作用。该文通过综述硝基化修饰蛋白质产生的途径及其在心血管疾病中促进内皮功能紊乱的可能机制,讨论了ROS/RNS介导的硝基化修饰与内皮功能障碍之间相互促进,共同推动心血管疾病进程的关系。该文还讨论了清除过氧亚硝酸盐、抑制ROS产生途径以及直接增强内皮细胞功能的治疗策略在内皮功能障碍相关的心血管疾病中的应用,可以为进一步研究蛋白质硝基化修饰这一蛋白质翻译后修饰作为干预靶点在心血管疾病中的作用提供参考。

Endothelial dysfunction,a common feature of various cardiovascular diseases,is closely associated with the overexpression of reactive oxygen species(ROS)/reactive nitrogen species(RNS).The reaction between superoxide anion and nitric oxide(NO)can generate peroxynitrite with stronger oxidation ability,which can deplete NO by oxidizing various proteins,leading to endothelial contraction and relaxation dysfunction,and playing an important role in various cardiovascular diseases.This article reviews the pathways through which nitrosylation modified proteins are produced and the possible mechanisms by which they promote endothelial dysfunction in cardiovascular disease.It discusses the relationship between ROS/RNS mediated nitrosylation modification and endothelial dysfunction,which together promote the progression of cardiovascular disease.The article also discusses the application of therapeutic strategies such as clearing peroxynitrite,inhibiting ROS production pathways,and directly enhancing endothelial cell function in cardiovascular diseases related to endothelial dysfunction,which can provide reference for further research on the role of protein nitration modification as a post-translational intervention target in cardiovascular diseases.