Matches in SemOpenAlex for { <https://semopenalex.org/work/W622339249> ?p ?o ?g. }
Showing items 1 to 53 of
53
with 100 items per page.
- W622339249 endingPage "127" @default.
- W622339249 startingPage "117" @default.
- W622339249 abstract "动脉粥样硬化、糖尿病、慢性肾功能衰竭和先兆子痫等血管疾病时活性氧（reactive oxygen species,ROS）生成增加,容易导致内皮依赖性血管舒张功能的损害和血管损伤,而细胞可以诱导多种编码Ⅱ相解毒酶和抗氧化蛋白的基因表达,从而减轻ROS和亲电子物质介导的细胞损伤。一个被称为抗氧化反应元件（antioxidant response element,ARE）或亲电子反应元件（electrophile response element,EpRE）的顺式转录调控元件,可以介导诸如亚铁血红素加氧酶1、γ-谷氨酰半胱氨酸合成酶、硫氧还蛋白还原酶、谷胱甘肽-S转移酶和NAD（P）H：苯醌氧化还原酶等基因的转录。其他抗氧化酶,如超氧化物歧化酶、过氧化氢酶和非酶清除剂（如谷胱甘肽）等也参与ROS的清除。转录因子NF-E2相关因子2（nuclear factor-erythroid 2-related factor 2, Nrf2）是属于Cap‘n’Collar家族的转录因子,具有碱性亮氨酸拉链（basic region-leucine zipper,bZIP）,它在ARE介导的抗氧化基因表达中起重要的作用。在正常情况下,Kelch样环氧氯丙烷相关蛋白-1（Kelch-like ECH-associated protein-1,Keapl）与Nrf2耦联,并与肌动蛋白细胞骨架结合被锚定于胞浆,但是在半胱氨酸残基发生氧化的情况下,Nrf2和Keapl解耦联,进入细胞核并与ARE结合,从而激活多种抗氧化基因和Ⅱ相解毒酶基因的转录。蛋白激酶C、丝裂原活化蛋白激酶和磷脂酰肌醇-3激酶参与Nrf2／ARE信号转导的调控。本文综述了有关Nrf2／ARE信号转导通路在血管稳态和动脉硬化、先兆子痫等疾病情况下内皮及平滑肌细胞对抗持续性氧化应激中起的作用。" @default.
- W622339249 created "2016-06-24" @default.
- W622339249 creator A5006454501 @default.
- W622339249 creator A5009191583 @default.
- W622339249 creator A5009685589 @default.
- W622339249 creator A5010503984 @default.
- W622339249 creator A5012743981 @default.
- W622339249 creator A5017361229 @default.
- W622339249 creator A5021635210 @default.
- W622339249 creator A5025778920 @default.
- W622339249 creator A5026635370 @default.
- W622339249 creator A5027948034 @default.
- W622339249 creator A5028444052 @default.
- W622339249 creator A5039962562 @default.
- W622339249 creator A5052970883 @default.
- W622339249 creator A5062039215 @default.
- W622339249 date "2007-01-01" @default.
- W622339249 modified "2023-10-07" @default.
- W622339249 title "内皮细胞和平滑肌细胞氧化应激时Nrf2／ARE信号通路对抗氧化基因表达的调控：与动脉粥样硬化和先兆子痫的关系" @default.
- W622339249 hasPublicationYear "2007" @default.
- W622339249 type Work @default.
- W622339249 sameAs 622339249 @default.
- W622339249 citedByCount "0" @default.
- W622339249 crossrefType "journal-article" @default.
- W622339249 hasAuthorship W622339249A5006454501 @default.
- W622339249 hasAuthorship W622339249A5009191583 @default.
- W622339249 hasAuthorship W622339249A5009685589 @default.
- W622339249 hasAuthorship W622339249A5010503984 @default.
- W622339249 hasAuthorship W622339249A5012743981 @default.
- W622339249 hasAuthorship W622339249A5017361229 @default.
- W622339249 hasAuthorship W622339249A5021635210 @default.
- W622339249 hasAuthorship W622339249A5025778920 @default.
- W622339249 hasAuthorship W622339249A5026635370 @default.
- W622339249 hasAuthorship W622339249A5027948034 @default.
- W622339249 hasAuthorship W622339249A5028444052 @default.
- W622339249 hasAuthorship W622339249A5039962562 @default.
- W622339249 hasAuthorship W622339249A5052970883 @default.
- W622339249 hasAuthorship W622339249A5062039215 @default.
- W622339249 hasConcept C144133560 @default.
- W622339249 hasConcept C41008148 @default.
- W622339249 hasConceptScore W622339249C144133560 @default.
- W622339249 hasConceptScore W622339249C41008148 @default.
- W622339249 hasIssue "2" @default.
- W622339249 hasLocation W6223392491 @default.
- W622339249 hasOpenAccess W622339249 @default.
- W622339249 hasPrimaryLocation W6223392491 @default.
- W622339249 hasVolume "59" @default.
- W622339249 isParatext "false" @default.
- W622339249 isRetracted "false" @default.
- W622339249 magId "622339249" @default.
- W622339249 workType "article" @default.