磷脂酶C参与去甲肾上腺素诱导的心肌细胞肥厚反应

Q4 Medicine
P. Tappia, V. Elimban, N. Dhalla
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引用次数: 1

摘要

已知去甲肾上腺素(NE)通过G蛋白偶联a1 -肾上腺素受体(a1 -AR)和磷酸化肌醇特异性磷脂酶C (PLC)的激活介导心肌细胞肥大。由于PLC活性的副产物是心脏肥厚的重要下游信号转导,因此本文重点介绍了PLC同工酶激活在心脏肥厚中的作用和调控机制。讨论的重点是强调PLC在不同的心脏肥大实验模型中,以及在用NE处理的分离的成人和新生儿心肌细胞中。特别强调的是关于a1 - ar - plc介导的肥厚信号通路。从所提供的信息来看,很明显,PLC同工酶的特异性激活是a1 -AR介导的NE反应以及心肌肥厚的开始和进展中的主要信号事件。此外,还描述了PLC参与心脏肥厚持续存在的可能性。这表明,特定的PLC同工酶可能作为预防心力衰竭高危患者人群心脏肥厚的可行靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Involvement of phospholipase C in the norepinephrine-induced hypertrophic response in Cardiomyocytes
Norepinephrine (NE) is known to mediate cardiomyocyte hypertrophy through the G protein coupled a1 -adrenoceptor (a1 -AR) and the activation of the phosphoinositide-specific phospholipase C (PLC). Since the by-products of PLC activity are important downstream signal transducers for cardiac hypertrophy, the role of and the regulatory mechanisms involved in the activation of PLC isozymes in cardiac hypertrophy are highlighted in this review. The discussion is focused to underscore PLC in different experimental models of cardiac hypertrophy, as well as in isolated adult and neonatal cardiomyocytes treated with NE. Particular emphasis is laid concerning the a1 -AR-PLC-mediated hypertrophic signalling pathway. From the information provided, it is evident that the specific activation of PLC isozymes is a primary signalling event in the a1 -AR mediated response to NE as well as initiation and progression of cardiac hypertrophy. Furthermore, the possibility of PLC involvement in the perpetuation of cardiac hypertrophy is also described. It is suggested that specific PLC isozymes may serve as viable targets for the prevention of cardiac hypertrophy in patient population at-risk for the development of heart failure.
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来源期刊
CiteScore
0.60
自引率
0.00%
发文量
13
审稿时长
4 weeks
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