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Cell Death Dis:跨细胞器应激反应破坏促进庆大霉素诱导型蛋白毒性

2020-04-18 QQY MedSci原创

在急性肾损伤(AKI)中,氨基糖苷类的肾毒病占四分之一以上,该病经常导致药物停用。

在急性肾损伤(AKI)中,氨基糖苷类的肾毒病占四分之一以上,该病经常导致药物停用。

作为最常用的氨基糖苷类药物,庆大霉素是一种具有肾毒性的抗生素,主要靶向近端小管上皮细胞引起急性肾损伤(AKI)。在原核细胞中,庆大霉素可以通过不可逆地结合细菌核糖体30S亚基来抑制蛋白质的合成。同时也可引起真核细胞发生内质网(ER)应激反应,激活未折叠蛋白质反应(UPR)并破坏线粒体。

虽然目前已有广泛的研究,但对于庆大霉素诱导的肾细胞损伤的机制及有效疗法还不清楚。

在该研究中,研究人员通过筛选RNAi信号通路来确定庆大霉素诱导的细胞损伤的统一机制,并提出相应的治疗改善策略。

庆大霉素暴露的人近端肾小管细胞中的RNAi信号筛选分析结果表明,跨细胞器应激反应(CORE)、未折叠蛋白反应(UPR)及细胞分子伴侣是庆大霉素诱导损伤的主要靶标。

为验证这点,研究人员评估了庆大霉素对于CORE、UPR及细胞分子伴侣功能的影响,并测试了增强细胞分子伴侣含量的治疗效果。

庆大霉素早期暴露会破坏CORE,主要是通过提高ATP:ADP的比例,线粒体特异性的H2O2的积累,Drp-1介导的线粒体碎片化以及内质网-线粒体分解来引起的。 CORE的破坏先于以下生物学过程,包括可测量的全细胞氧化应激水平的增加、蛋白质折叠错误、UPR转录的激活及其不利的下游反应:CHOP的表达、PARP的裂解及细胞死亡。

 替普瑞酮(Geranylgeranylacetone)是一种治疗剂,可以增加细胞分子伴侣的含量,防止线粒体H2O2积累,保护CORE,减少蛋白质的错误折叠,降低CHOP表达负担并显著提高庆大霉素暴露细胞的存活率。

综上,该研究表明跨细胞器应激反应破坏是庆大霉素蛋白毒性的早期并可治疗的主要原因,其出现于下游UPR的激活及细胞死亡过程之前。通过减少庆大霉素暴露期间细胞器特异性蛋白毒性保护CORE免受破坏能够显著改善肾细胞的存活。

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    2020-12-07 docwu2019
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    2020-04-20 cy0328

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