Anti-inflammatory circuitry: Lipoxin, aspirin-triggered lipoxins and their receptor ALX
Anti-inflammatory circuitry: Lipoxin, aspirin-triggered lipoxins and their receptor ALX
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DOI：
10.1016/j.plefa.2005.05.003
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发表时间：
2005-09-01
影响因子：
3
通讯作者：
Serhan, CN
中科院分区：
文献类型：
--
作者：
Chiang, N;Arita, M;Serhan, CN
内源性化学介质或自体激素在控制炎症及其程序性消退中起关键作用。其中，已知脂氧素（LX）和阿司匹林触发的LX（ATL）在一系列生理和病理生理过程中引起生物作用，并作为内源性脂质/化学介质，阻止嗜中性粒细胞浸润并启动消退。LXA（4）、ATL及其代谢稳定的类似物通过与其特异性受体ALX相互作用，在体内引起细胞反应并调节PMN，ALX是第一个克隆和鉴定的具有细胞类型特异性信号通路的脂氧合酶衍生的类花生酸受体。此外，ALX可以通过在炎症反应的特定阶段与各类配体（脂质与肽）相互作用来调节PMN。LX、ATL和ALX一起可以提供新的机会来设计在控制炎症方面具有高度精确度的“分辨率靶向”疗法。在本章中，我们对LX和ATL的当前作用、ALX的鉴定及其新的抗炎和促消退信号进行了概述和更新。(c)2005爱思唯尔有限公司保留所有权利。
Endogenous chemical mediators or autacoids play key roles in controlling inflammation and its programmed resolution. Among them, it is known that lipoxins (LX) and aspirin-triggered LX (ATL) evoke bioactions in a range of physiologic and pathophysiologic processes and serve as endogenous lipid/chemical mediators that stop neutrophilic infiltration and initiate resolution. LXA(4), ATL and their metabolic stable analogs elicit cellular responses and regulate PMN in vivo via interacting with their specific receptor, namely ALX ALX is the first cloned and identified lipoxygenase-derived eicosanoid receptor with cell type-specific signaling pathways. Also, ALX could regulate PMN by interacting with each class of ligands (lipid vs. peptide) within specific phases of an inflammatory response. Together LX, ATL and ALX may provide new opportunities to design "resolution-targeted" therapies with high degree of precision in controlling inflammation. In this chapter, we give an overview and update of the current actions for LX and ATL, the identification of ALX and their novel anti-inflammatory and pro-resolving signals. (c) 2005 Elsevier Ltd. All rights reserved.