机构：[1]Eight-year Medical Doctor Program, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.[2]Department of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing, China.首都医科大学宣武医院神经科系统神经外科[3]Sir William Dunn School of Pathology, University of Oxford, Oxford, United Kingdom.[4]China International Neuroscience Institute (China-INI), Beijing, China.[5]First Hospital, Peking University, Beijing, China.[6]Laboratory of Computational Biology and Machine Intelligence, National Laboratory of Pattern Recognition, Institute of Automation, Chinese Academy of Sciences, Beijing, China.[7]School of Artificial Intelligence, University of Chinese Academy of Sciences, Beijing, China.[8]Department of Interventional Neuroradiology, Xuanwu Hospital, Capital Medical University, Beijing, China.首都医科大学宣武医院医技科室放射科
Various signaling pathways are regulated by reactive oxygen species (ROS), which are radical oxygen intermediates under normal physiological conditions. However, when the buffering capacity of antioxidant enzymes is exceeded by the accumulation of ROS, oxidative stress, and endothelial cell dysfunction occur, which have been recognized as key contributors to the development of atherosclerosis. In this review, an overview is provided on mechanisms underlying ROS generation in endothelial cells and the involved regulatory pathways. Further, we discuss the ROS induced endothelial cell dysfunction and its relationship with atherosclerosis. Current knowledge on ROS-induced endothelial impairment is presented, characterized by decreased NO bioavailability, intracellular dysfunction and ox-LDL accumulation. Furthermore, biomarkers such as oxidative products of lipid, protein, and nucleotide are discussed as measurements for ROS levels. Novel interventions targeting oxidative stress are listed as potential pharmacotherapies in clinical practice. In conclusion, this review presents a systematic analysis of the mechanisms underlying ROS generation and elucidates how manipulation of these mechanisms can safeguard endothelial cell function.
基金：
National Natural Science Foundation of China [82301468, 82171303]; Incubating Program of Capital Medical University [PYZ22041]; Beijing Hospitals Authority's Ascent Plan [DFL20220702]
第一作者机构：[1]Eight-year Medical Doctor Program, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
共同第一作者：
通讯作者：
通讯机构：[2]Department of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing, China.[4]China International Neuroscience Institute (China-INI), Beijing, China.[8]Department of Interventional Neuroradiology, Xuanwu Hospital, Capital Medical University, Beijing, China.[*1]Department of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing, China
推荐引用方式(GB/T 7714)：
Yan Ruiyi,Zhang Xiao,Xu Wenlong,et al.ROS-Induced Endothelial Dysfunction in the Pathogenesis of Atherosclerosis[J].AGING AND DISEASE.2025,doi:10.14336/AD.2024.0309.
APA：
Yan, Ruiyi,Zhang, Xiao,Xu, Wenlong,Li, Jiayao,Sun, Yixin...&Wang, Tao.(2025).ROS-Induced Endothelial Dysfunction in the Pathogenesis of Atherosclerosis.AGING AND DISEASE,,
MLA：
Yan, Ruiyi,et al."ROS-Induced Endothelial Dysfunction in the Pathogenesis of Atherosclerosis".AGING AND DISEASE .(2025)
