内质网应激介导的肾损伤及干预和保护策略

Endoplasmic Reticulum Stress-involved Kidney Damage and the Intervention and Protection Strategy against It

内质网应激是真核细胞对各种有害刺激的保护性应答机制,可触发以未折叠蛋白反应为核心的相关信号通路,且未折叠蛋白反应在内质网应激初期具有细胞保护作用,但在内质网应激过度(即过强或时间过长)时则会导致细胞程序性死亡。新近研究发现,内质网应激与多种肾毒物引发的肾损伤机制密切相关。本文通过简介内质网应激的相关信号通路及介导的细胞凋亡机制以及其生理病理学意义,并以若干典型肾毒物为例,着重对内质网应激在各类肾毒物引发肾损伤过程中的作用作一综述,探讨对内质网应激介导肾损伤的干预和保护策略。

Endoplasmic reticulum stress （ERS）, a self protection mechanism of eukaryotic cell against varieties of harmful stimuli, could activate the related signal pathways based on the unfolded protein response, which serves as an adaptive cytoprotection initially or leads to programmed cell death under severe or prolonged stress. Recent researches have revealed that the ERS is involved with mechanisms of kidney damage caused by nephrotoxicants. The ERS-related signal pathways, ERS-mediated apoptosis mechanism and physiopathological roles of ERS were briefly introduced. With some typical kidney toxicants as examples, the roles of ERS in kidney damage induced by different kidney toxicants were emphatically reviewed. The intervention and protection strategy against ERS-involved kidney damage was discussed.