Phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin signaling pathway and epilepsy
10.3760/cma.j.issn.2095-428X.2015.24.020
- VernacularTitle:磷脂酰肌醇3-激酶/蛋白激酶B/哺乳动物西罗莫司靶蛋白信号通路与癫(痫)
- Author:
Qinrui LI
;
Jiong QIN
;
Junbao DU
;
Ying HAN
;
Hongfang JIN
;
Yang ZHAO
;
Jing ZHANG
- Publication Type:Journal Article
- Keywords:
Phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin signaling pathway;
Epilepsy;
Rapamycin
- From:
Chinese Journal of Applied Clinical Pediatrics
2015;30(24):1915-1917
- CountryChina
- Language:Chinese
-
Abstract:
Study of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling pathway has been becoming more and more popular.This pathway widely exists in kinds of cells of human being.As one main anti-apoptic and enhancing survival pathway in cells, it plays an important role in cellular growth (increased cell size), proliferation (increased cell number), apoptosis, cell survival and migration.At the same time,the pathway regulates many major cellular processes and is implicated in an increasing number of pathological conditions, including cancer, obesity, type 2 diabetes, and neurodegeneration disease, epilepsy.In recent years,many studies have shown that the dysfunction of PI3K/Akt/mTOR signaling pathway can lead to neurodevelopmental disease.Loss of tuberous sclerosis complex (TSC)1/2 or phosphatase ad tensin homologue deleted on chromosome 10 (PTEN), or environmental stimuli such as inflammation, epilepsy, or hypoxia may stimulate mTOR-dependent protein synthesis,resulting in a host of cellular, structural, and physiological responses that culminate in clinical symptoms.Study the role of mTOR signaling pathway in early-onset epileptic encephalopathy, discuss the intervention and therapy in early-onset epileptic encephalopathy have important clinical meanings.In this article, the components, physiological functions,information were elucidated relative to the PI3 K/Akt/mTOR signaling pathway, and the interaction of the signaling pathway and epilepsy was discussed.
