Nuclear receptors and inflammation control: molecular mechanisms and pathophysiological relevance.

Nuclear receptors and inflammation control: molecular mechanisms and pathophysiological relevance.
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DOI:
10.1161/atvbaha.109.191189
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发表时间:
2010-08
期刊:
Arteriosclerosis, thrombosis, and vascular biology
影响因子:
--
通讯作者:
Glass CK
Glass CK
中科院分区:
其他
文献类型:
--
作者:
Huang W;Glass CK

文献摘要

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组织炎症是一个严格调节的过程,通常用于将免疫系统招募到感染和损伤部位,并促进组织修复过程。当炎症状态过度或延长时,对宿主组织的局部和全身损伤可导致正常生理功能的丧失。在这里,我们简要回顾了最近的研究,推进我们的理解,在转录水平和反调节这些途径的核受体超家族的选定成员参与启动炎症反应的信号通路。核受体和炎症的交叉研究揭示了正和负转录控制机制,这可能为动脉粥样硬化等慢性疾病的药物干预提供新的靶点。
Tissue inflammation is a tightly regulated process that normally serves to recruit the immune system to sites of infection and injury and to facilitate tissue repair processes. When an inflammatory state is excessive or prolonged, local and systemic damage to host tissues can result in loss of normal physiological functions. Here, we briefly review recent studies that advance our understanding of signaling pathways involved in initiation of inflammatory responses at the level of transcription and counter-regulation of these pathways by selected members of the nuclear receptor superfamily. Studies of the intersection of nuclear receptors and inflammation have revealed mechanisms of positive and negative transcriptional control that may provide new targets for pharmacological intervention in chronic diseases such as atherosclerosis.