[1]李慧丹,赵文鸽,王学惠.Nox4在同型半胱氨酸介导的动脉粥样硬化中作用的研究[J].医学信息,2019,32(15):45-47.[doi:10.3969/j.issn.1006-1959.2019.15.015]
　LI Hui-dan,ZHAO Wen-ge,WANG Xue-hui.Research on the Role of Nox4 in Homocysteine-mediated Atherosclerosis[J].Journal of Medical Information,2019,32(15):45-47.[doi:10.3969/j.issn.1006-1959.2019.15.015]
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Nox4在同型半胱氨酸介导的动脉粥样硬化中作用的研究()
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医学信息[ISSN:1006-1959/CN:61-1278/R]

卷:
32卷
期数:
2019年15期
页码:
45-47
栏目:
综述
出版日期:
2019-08-01

文章信息/Info

Title:
Research on the Role of Nox4 in Homocysteine-mediated Atherosclerosis
文章编号:
1006-1959（2019）15-0045-03
作者:
李慧丹; 赵文鸽; 王学惠
新乡医学院第一附属医院心血管内科，河南 卫辉 453100
Author(s):
LI Hui-dan; ZHAO Wen-ge; WANG Xue-hui
Department of Cardiology,the First Affiliated Hospital of Xinxiang Medical College,Weihui 453100,Henan,China
关键词:
同型半胱氨酸; 动脉粥样硬化; Nox4; NLRP3
Keywords:
Key words：Homocysteine; Atherosclerosis; Nox4; NLRP3
分类号:
R543.5
DOI:
10.3969/j.issn.1006-1959.2019.15.015
文献标志码:
A
摘要:
同型半胱氨酸（Hcy）是心血管疾病的独立危险因子之一。Hcy能够诱导细胞活性氧（ROS）的生成增多引起内皮损伤从而导致动脉粥样硬化（AS）发生发展。内皮细胞中ROS主要来源于Nox4（NADPH oxidases 4）。NLRP3在冠状动脉粥样硬化及主动脉硬化中高表达。NLRP3是AS中IL-1家族细胞因子产生的关键介质，特别是当细胞内产生的大量ROS，可导致caspase-1前体大量剪切成具有生物活性的caspase-1 P10片段，推动下游IL-1β和IL-18等炎症因子的成熟及分泌，使内皮细胞功能受损，引起细胞炎症损伤及凋亡，正反馈加重血管损伤。本文主要探讨Nox4在Hcy介导的内皮细胞炎症及凋亡的作用，Hcy导致的AS提供可能的机制。
Abstract:
Abstract：Homocysteine (Hcy) is one of the independent risk factors for cardiovascular disease. Hcy can induce the increase of cellular reactive oxygen species (ROS) to cause endothelial damage leading to the development of atherosclerosis (AS). ROS in endothelial cells are mainly derived from Nox4 (NADPH oxidases 4). NLRP3 is highly expressed in coronary atherosclerosis and aortic sclerosis. NLRP3 is a key mediator of IL-1 family cytokine production in AS, especially when a large amount of ROS produced in cells can cause a large amount of caspase-1 precursor to be cleaved into a biologically active caspase-1 P10 fragment,promote the maturation and secretion of downstream inflammatory factors such as IL-1β and IL-18, impair endothelial cell function, cause cell inflammatory damage and apoptosis, and positive feedback aggravates vascular injury. This study focuses on the role of Nox4 in Hcy-mediated endothelial cell inflammation and apoptosis, and Hcy-induced AS provides a possible mechanism.

参考文献/References:

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更新日期/Last Update: 2019-08-01