Huang Zixia, Wu Mingyue, Zeng Lijin, Wang Deming
Department of Anesthesiology, The Second Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan 421001, China.
Department of Emergency, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510080, China.
Cardiol Res Pract. 2022 May 12;2022:4287711. doi: 10.1155/2022/4287711. eCollection 2022.
Cardiovascular disease (CVD) is a serious public health issue in China, accounting for more than 40% of all mortality, and it is the leading cause of death worldwide. Atherosclerosis is the pathological basis for much CVD, including coronary heart disease, acute myocardial infarction, and stroke. Endothelial dysfunction is an initiating and exacerbating factor in atherosclerosis. Recent research has linked oxidative stress and mitochondrial damage to endothelial dysfunction. Nuclear factor erythroid 2-related factor 2 (Nrf2) is a transcription factor with antioxidant effects that is strongly connected to several CVDs. However, the mechanism by which Nrf2 reduces CVD is unknown. Research indicates that Nrf2 improves endothelial function by resisting oxidative stress and mitochondrial damage, thereby delaying atherosclerosis. This article examines the mechanisms and potential targets of Nrf2 affecting endothelial cell function to improve atherosclerosis and to provide ideas for the development of new CVD treatments.
心血管疾病（CVD）在中国是一个严重的公共卫生问题，占总死亡率的40%以上，并且是全球主要的死亡原因。动脉粥样硬化是许多心血管疾病的病理基础，包括冠心病、急性心肌梗死和中风。内皮功能障碍是动脉粥样硬化的起始和加剧因素。最近的研究将氧化应激和线粒体损伤与内皮功能障碍联系起来。核因子红细胞2相关因子2（Nrf2）是一种具有抗氧化作用的转录因子，与多种心血管疾病密切相关。然而，Nrf2降低心血管疾病的机制尚不清楚。研究表明，Nrf2通过抵抗氧化应激和线粒体损伤来改善内皮功能，从而延缓动脉粥样硬化。本文探讨Nrf2影响内皮细胞功能以改善动脉粥样硬化的机制和潜在靶点，为开发新的心血管疾病治疗方法提供思路。
