细胞焦亡发生机制及其相关疾病的研究进展
石明霞;谢美玉;郭顺利;周素芳;
摘要(Abstract):
细胞焦亡是一种由Gasdermin介导的程序性细胞坏死,表现为细胞肿胀、破裂,内容物释出并伴随强烈的炎症反应。病原体入侵时,机体通过一定途径促使炎症小体形成,进而激活依赖胱天蛋白酶1(Caspase-1)的经典细胞焦亡通路和/或依赖Caspase-4/5/11的非经典细胞焦亡通路。活化的Caspase-1/4/5/11将底物蛋白GSDMD切割为有成孔活性的N末端和有自抑作用的C末端,GSDMD-N通过成孔活性介导细胞焦亡。GSDME在Caspase-3的切割作用下能将TNF-α诱导的细胞凋亡转换为细胞焦亡,且能增加化疗药物的活性,但亦与不良反应密切相关。诸多疾病伴随有细胞焦亡现象的发生,如感染性疾病、痛风、免疫缺陷疾病、自身免疫性疾病等。
关键词(KeyWords): 细胞焦亡;炎症小体;GSDMD蛋白;GSDME蛋白
基金项目(Foundation): 国家自然科学基金资助项目(S1460432);; 广西自然科学基金资助项目(2015GXNSFDA139017)
作者(Authors): 石明霞;谢美玉;郭顺利;周素芳;
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