内质网钙稳态与内质网应激  

ER Ca^(2+)homeostasis and ER stress

作　　者：赵松 刘红美 唐铁山[1,2,3] ZHAO Song;LIU HongMei;TANG Tie-Shan(State Key Laboratory of Membrane Biology,Key Laboratory of Organ Regeneration and Reconstruction,Institute of Zoology,Chinese Academy of Sciences,Beijing 100101,China;University of Chinese Academy of Sciences,Beijing 100101,China;Beijing Institute for Stem Cell and Regenerative Medicine,Beijing 100101,China)

机构地区：[1]中国科学院动物研究所,膜生物学国家重点实验室,器官再生与智造重点实验室,北京100101 [2]中国科学院大学,北京100101 [3]北京干细胞与再生医学研究院,北京100101

出　　处：《中国科学：生命科学》2024年第8期1318-1326,共9页Scientia Sinica(Vitae)

基　　金：国家自然科学基金(批准号:92254301,82030033,81921006,32070780)资助。

摘　　要：维持内质网(endoplasmic reticulum, ER)中Ca^(2+)存储的稳态对于准确的Ca^(2+)信号传导和关键的细胞功能至关重要.内质网作为细胞内Ca^(2+)的主要存储介质,对蛋白质折叠、分泌和Ca^(2+)稳态十分重要.内质网Ca^(2+)耗竭诱导内质网应激已被广泛认可,但是关于Ca^(2+)耗竭诱导内质网应激的机制目前尚不十分清楚;此外内质网Ca^(2+)过载是否会诱导内质网应激反应也知之甚少.本文总结了内质网钙稳态与内质网应激通路相关研究的最新进展.Maintaining homeostasis of Ca^(2+)stores in the endoplasmic reticulum(ER)is crucial for proper Ca^(2+)signaling and key cellular functions.ER,the main intracellular storage medium for Ca^(2+),is essential for protein folding,secretion,and Ca^(2+)homeostasis.Ca^(2+)depletion induced ER stress has been widely recognized,but the mechanism of ER stress induced by Ca^(2+)depletion has not been well resolved,and little is known whether ER Ca^(2+)overload could induce ER stress.Here,we summarize the latest progress in the ER Ca^(2+)homeostasis and the induction of ER stress.

关 键 词：钙稳态 Ca^(2+)耗竭 内质网钙过载 内质网应激 

分 类 号：Q244[生物学—细胞生物学]