新型酪氨酸激酶信号通路：对血管重构的影响。
Novel tyrosine kinase signaling pathways: implications in vascular remodeling.
机构信息
Department of Medicine, Aab Cardiovascular Research Institute, University of Rochester School of Medicine and Dentistry, Rochester, New York, USA.
出版信息
Curr Opin Nephrol Hypertens. 2012 Mar;21(2):122-7. doi: 10.1097/MNH.0b013e3283503ce9.
Abstract
PURPOSE OF REVIEW
This review summarizes the recent advances in molecular mechanisms by which five classes of receptor tyrosine kinases (RTKs) contribute to vascular remodeling.
RECENT FINDINGS
Recent findings have expanded our knowledge regarding RTK regulation. In particular, G-protein-coupled receptors, mineralocorticoid receptors, mechanical and oxidative stresses transactivate RTKs. These receptors are highly interactive with many downstream targets (including tyrosine kinases and other RTKs) and function as key regulatory nodes in a dynamic signaling network. Interactions between vascular and nonvascular (immune and neuronal) cells are controlled by RTKs in vascular remodeling. Inhibition of RTKs could be an advantageous therapeutic strategy for vascular disorders.
SUMMARY
RTK-dependent signaling is important for regulation of key functions during vascular remodeling. However, current challenges are related to integration of the data on multiple RTKs in vascular pathology.
摘要
目的综述
本文总结了五类受体酪氨酸激酶（RTKs）在血管重构中发挥作用的分子机制的最新进展。
最近的发现
最近的发现扩展了我们对 RTK 调节的认识。特别地，G 蛋白偶联受体、盐皮质激素受体、机械和氧化应激可转激活 RTKs。这些受体与许多下游靶标（包括酪氨酸激酶和其他 RTKs）高度相互作用，并作为动态信号网络中的关键调节节点发挥作用。血管和非血管（免疫和神经元）细胞之间的相互作用受血管重构中 RTKs 的控制。抑制 RTKs 可能是治疗血管疾病的有利策略。
总结
RTK 依赖性信号对于血管重构过程中关键功能的调节很重要。然而，目前的挑战与整合血管病理学中多个 RTKs 的数据有关。
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