Ca(2+) Ion and Autophagy
Ca(2+) Ion and Autophagy
复制标题
DOI：
10.1007/978-981-15-0602-4_7
复制
发表时间：
2019-01-01
期刊：
影响因子：
--
通讯作者：
Jing, Qing
中科院分区：
文献类型：
--
作者：
Hu, Yang-Xi;Han, Xiao-Shuai;Jing, Qing
细胞内钙离子（Ca（2+））受严格的机制控制，与细胞的各种活动密切相关，其中包括自噬的调节。研究者认为，在正常或应激状态下，Ca（2+）对细胞自噬具有正、负调节作用，其调节机制各不相同。Ca（2+）在不同条件下对自噬的双向调节作用（促进或抑制）仍存在争议，其可能机制也存在争议。研究表明，Ca（2+）通过多种途径促进自噬，如1，4，5-三磷酸肌醇受体（IP 3R）和beclin 1途径，钙调素依赖性激酶β（CaM β）途径，（CaMKK beta）-AMPK-mTOR通路，线粒体能量代谢相关的Ca（2+）摄取，溶酶体对Ca（2+）信号的调节，也有人认为Ca（2+）可能通过IP 3R、Beclin 1-Bcl-2复合物和AMPK-mTOR途径抑制自噬。要彻底了解Ca（2+）和自噬的真相，似乎还有很长的路要走。
Controlled by a strict mechanism, intracellular calcium (Ca(2+)) is closely related to various cellular activities, including the regulation of autophagy. Researchers believed that under normal or stress state, Ca(2+) has a positive or negative regulation effect on autophagy, the mechanisms of which are different. This bidirectional role of Ca(2+), promotive or suppressing in the regulation of autophagy under different conditions remains controversial, so as the potential mechanisms. Several studies reported that Ca(2+) promotes autophagy through plenty of ways, like inositol 1,4,5-trisphosphate receptor (IP3R) and beclin1 pathway, calmodulin-dependent kinase kinase beta (CaMKK beta)-AMPK-mTOR pathway, mitochondrial energy metabolism-related Ca(2+) uptake, lysosome's regulation of Ca(2+) signal, and so on. Others thought Ca(2+) may inhibit autophagy through IP3R and beclin1-Bcl-2 complex and the AMPK-mTOR pathway, either. It seems to be still a long way to thoroughly understand the truth of Ca(2+) and autophagy.