自噬
安普克
细胞生物学
PI3K/AKT/mTOR通路
溶酶体
化学
肌醇
ULK1
激酶
袋3
蛋白激酶A
信号转导
生物
受体
生物化学
细胞凋亡
酶
作者
Yang-Xi Hu,Xiao-Shuai Han,Qing Jing
标识
DOI:10.1007/978-981-15-0602-4_7
摘要
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 (CaMKKβ)–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.
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