摘要
近年来,哺乳动物雷帕霉素靶蛋白(mTOR)研究方面的重大进展,大大增强了我们对mTOR在控制细胞过程中的作用和细胞通路的理解,如翻译起始,肌动蛋白的组织,细胞增殖,细胞存活等。mTOR激活主要是通过mTOR复合物1或mTOR复合体2的磷酸化作用。mTORC1激活是通过结节性硬化症一半依赖和一半独立的刺激机制,由生长因子,营养素,氨基酸和其它信号通路进行刺激。mTOR的活性与细胞增殖和分化,凋亡和自噬密切相关。活化的mTOR通过调节其多靶点阻止细胞凋亡和自噬。鉴于mTOR活性参与了神经退行性疾病,心血管畸形,代谢性疾病,肾移植,自身免疫异常和癌症,通过调节mTOR活性方式,可能作为这些疾病的一种新的治疗策略。然而,mTOR在体内的作用很复杂,因此,其活性需要严格控制,以便在特定的病理条件下取得有利的结果。
关键词: 蛋白激酶,心血管疾病,糖尿病,mTOR,神经变性疾病
图形摘要
Current Drug Targets
Title:mTOR: A Novel Therapeutic Target for Diseases of Multiple Systems
Volume: 16 Issue: 10
Author(s): Zhao Zhong Chong
Affiliation:
关键词: 蛋白激酶,心血管疾病,糖尿病,mTOR,神经变性疾病
摘要: Significant progress in the research of mammalian target of rapamycin (mTOR) in recent years, has greatly enhanced our understanding of the role and cellular pathways through which mTOR control cellular processes, such as translational initiation, actin organization, cell proliferation, and cell survival. mTOR is activated by phosphorylation and functions mainly through mTOR complex 1 or mTOR complex 2. mTORC1 is activated through tuberous sclerosis complex 1/2 dependent and independent mechanisms following the stimulation by growth factors, nutrient, amino acids, and other signaling pathways. The activity of mTOR is closely associated with cell proliferation and differentiation, apoptosis, and autophagy. Activation of mTOR prevents the induction of both apoptosis and autophagy through regulating its multiple targets. Given that the activity of mTOR has been involved in the pathogenesis of neurodegenerative disorders, cardiovascular abnormalities, metabolic diseases, renal transplantation, autoimmune abnormalities, and cancer, manipulating mTOR activation may represent as an innovative therapeutic strategy for these diseases. Yet, the role of mTOR in the body is complicated and therefore, its activity needs to be tightly regulated to achieve beneficial outcome in a specific pathological condition.
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Cite this article as:
Zhao Zhong Chong , mTOR: A Novel Therapeutic Target for Diseases of Multiple Systems, Current Drug Targets 2015; 16 (10) . https://dx.doi.org/10.2174/1389450116666150408103448
DOI https://dx.doi.org/10.2174/1389450116666150408103448 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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