热休克蛋白在动脉粥样硬化中的作用研究进展

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热休克蛋白(HSP)是一组进化高度保守的蛋白质,普遍存在于从细菌到人类的整个生物界.最早是Ritossa于1962年从热诱导的果蝇染色体上看到蓬松现象,提示这些区域带基因的转录加强并可能有某些蛋白质的合成增加.至1974年,Tissieres等才从热休克果蝇染色体幼虫的唾液腺等部位分离到新的蛋白质,并正式命名为HSP.后来认识到除了高温外,其他因素(包括感染、组织创伤、氧化应激、营养缺乏、中毒等)均能诱导细胞生成HSP,因此HSP又称做应激蛋白.但HSP家族中有部分成员在正常生理状态下也有表达.HSP的主要生理功能是作为细胞的蛋白质分子伴侣,可以描述为"蛋白质结构的催化剂".此外,HSP在细胞周期调控、细胞增殖、组织的细胞结构、细胞凋亡中发挥作用.因此HSP在动脉粥样硬化(AS)中起作用也就不足为奇了.分子模拟或种间交叉反应表明,T细胞、B细胞反应的病理学机制已经证明HSP与各种炎症及自身免疫反应(包括AS)相关[1].
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