Toll-like receptors in atherosclerosis.

Toll-like receptors in atherosclerosis.
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DOI:
10.3390/ijms140714008
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发表时间:
2013-07-04
影响因子:
5.6
通讯作者:
Monaco C
Monaco C
中科院分区:
生物学2区
文献类型:
--
作者:
Falck-Hansen M;Kassiteridi C;Monaco C

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动脉粥样硬化是心血管疾病(CVD)的主要原因,由炎症驱动。越来越多的证据表明,Toll样受体(TLR)是动脉粥样硬化疾病过程的关键协调。有趣的是,动脉粥样硬化中的个体受体显示了一幅独特的画面。TLR表现出复杂的性质,使得能够检测称为病原体相关分子模式(DAMP)和病原体相关分子模式(PAMP)的多个基序。这些受体的激活触发通过MyD88或TRIF介导的细胞内信号级联,导致促炎和抗炎细胞因子的产生。在这篇综述中,我们探讨了与动脉粥样硬化TLR信号转导有关的关键新发现,包括最近描述的内体TLR和TLR研究的未来方向。
Atherosclerosis, the leading cause of cardiovascular disease (CVD), is driven by inflammation. Increasing evidence suggests that toll-like receptors (TLRs) are key orchestrators of the atherosclerotic disease process. Interestingly, a distinct picture is being revealed for individual receptors in atherosclerosis. TLRs exhibit a complex nature enabling the detection of multiple motifs named danger-associated molecular patterns (DAMPs) and pathogen-associated molecular patterns (PAMPs). Activation of these receptors triggers an intracellular signalling cascade mediated through MyD88 or TRIF, leading to the production of pro- and anti-inflammatory cytokines. In this review we explore key novel findings pertaining to TLR signalling in atherosclerosis, including recently described endosomal TLRs and future directions in TLR research.
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