摘要
背景:Ca2 +流入在几种神经系统疾病的生理和病理生理过程中起重要作用。瞬时受体电位通道(TRPCs)形成一系列电压敏感的钙离子通道。 目的:在本次综述中,我们将讨论临床受体潜能规范(TRPC)通道的重要性,这是一个至关重要的钙通道家族。本文回顾了TRPC通道在脑出血,脑梗死后出血性转化,蛛网膜下腔出血和脑损伤等疾病发病机制中的作用。 结果:TRPC在中枢神经系统(CNS)中表达特别高,涉及几种生理功能。 TRPC家族与蛛网膜下腔出血后脑血管痉挛,脑内出血后神经元损伤,脑缺血后NMDA细胞毒性,神经系统肿瘤,神经退行性疾病,神经痴呆等疾病有关。 结论:TRPC家族功能丰富,分布广泛,各种神经系统疾病功能不同。
关键词: 脑损伤,Ca2 +,出血性转化,脑内出血,神经系统,蛛网膜下腔出血,TRPCs。
图形摘要
Current Drug Targets
Title:Targeting Transient Receptor Potential Canonical Channels for Diseases of the Nervous System
Volume: 18 Issue: 12
关键词: 脑损伤,Ca2 +,出血性转化,脑内出血,神经系统,蛛网膜下腔出血,TRPCs。
摘要: Background: Ca2+ influx plays an essential role in the physiological and pathophysiologic processes of several nervous system diseases. The transient receptor-potential channels (TRPCs) form a family of voltage –sensitive calcium ion channels.
Objective: In this review, we will discuss the importance of transient receptor potential canonical (TRPC) channels, which is a crucial family of calcium channels. This article reviews the role of TRPC channels in the pathogenesis of diseases such as brain hemorrhage, hemorrhagic transformation after cerebral infarction, subarachnoid hemorrhage, and brain injury. Results: TRPC has especially high expression in the central nervous system (CNS), and was involved in several physiological functions. The TRPC family is associated with cerebral vasospasm after subarachnoid hemorrhage, neuronal damage after intracerebral hemorrhage, NMDA cytotoxicity in cerebral ischemia, nervous system tumors, neurodegenerative diseases, neural addiction and other diseases. Conclusion: The TRPC family has rich functionality and is widely distributed, with different functions in various nervous system diseases.Export Options
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Cite this article as:
Targeting Transient Receptor Potential Canonical Channels for Diseases of the Nervous System, Current Drug Targets 2017; 18 (12) . https://dx.doi.org/10.2174/1389450117666151209120007
DOI https://dx.doi.org/10.2174/1389450117666151209120007 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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