神经发生
PI3K/AKT/mTOR通路
医学
缺血
神经科学
神经干细胞
再生(生物学)
血管生成
冲程(发动机)
神经保护
干细胞
癌症研究
信号转导
细胞生物学
生物
内科学
机械工程
工程类
作者
Jiale Gao,Mingjiang Yao,Dennis Chang,Jianxun Liu
出处
期刊:Stroke
[Ovid Technologies (Wolters Kluwer)]
日期:2023-01-01
卷期号:54 (1): 279-285
被引量:13
标识
DOI:10.1161/strokeaha.122.040376
摘要
Ischemic stroke remains a leading cause of morbidity and disability around the world. The sequelae of serious neurological damage are irreversible due to body's own limited repair capacity. However, endogenous neurogenesis induced by cerebral ischemia plays a critical role in the repair and regeneration of impaired neural cells after ischemic brain injury. mTOR (mammalian target of rapamycin) kinase has been suggested to regulate neural stem cells ability to self-renew and differentiate into proliferative daughter cells, thus leading to improved cell growth, proliferation, and survival. In this review, we summarized the current evidence to support that mTOR signaling pathways may enhance neurogenesis, angiogenesis, and synaptic plasticity following cerebral ischemia, which could highlight the potential of mTOR to be a viable therapeutic target for the treatment of ischemic brain injury.
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