Regulation of platelet function by class B scavenger receptors in hyperlipidemia.

Regulation of platelet function by class B scavenger receptors in hyperlipidemia.
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高脂血症中 B 类清道夫受体对血小板功能的调节。

DOI:
10.1161/atvbaha.110.207498
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发表时间:
2010
期刊:
Arteriosclerosis, thrombosis, and vascular biology
影响因子:
--
通讯作者:
Podrez,EugeneA
Podrez,EugeneA
中科院分区:
--
文献类型:
--
作者:
Zimman,Alejandro;Podrez,EugeneA

文献摘要

相似文献

血小板组成型表达B类清道夫受体CD 36和SR-BI,这两种密切相关的模式识别受体因其在脂蛋白和脂质代谢中的作用而闻名。血小板中清道夫受体的生物学作用知之甚少。然而,在体外和体内的数据表明,B类清道夫受体调节血小板功能,并有助于显着血栓形成的病理或生理配体,诱导血栓前信号,并增加血小板的反应性。血小板CD 36识别一个新的内源性氧化胆碱磷脂家族,该家族在高脂血症小鼠血浆和低高密度脂蛋白水平受试者血浆中蓄积。这种相互作用导致特定信号通路的激活,并促进血小板活化和血栓形成。另一方面,在与血小板胆固醇含量增加相关的条件下,血小板SR-BI在诱导血小板高反应性和加速血栓形成中起关键作用。有趣的是,氧化高密度脂蛋白,一种SR-BI配体,可以抑制血小板功能。这些最新的研究结果表明,血小板B类清道夫受体在血脂异常的血栓形成中发挥作用,并可能有助于体内高胆固醇血症的急性心血管事件。
Platelets constitutively express class B scavenger receptors CD36 and SR-BI, 2 closely related pattern recognition receptors best known for their roles in lipoprotein and lipid metabolism. The biological role of scavenger receptors in platelets is poorly understood. However, in vitro and in vivo data suggest that class B scavenger receptors modulate platelet function and contribute significantly to thrombosis by sensing pathological or physiological ligands, inducing prothrombotic signaling, and increasing platelet reactivity. Platelet CD36 recognizes a novel family of endogenous oxidized choline phospholipids that accumulate in plasma of hyperlipidemic mice and in plasma of subjects with low high-density lipoprotein levels. This interaction leads to the activation of specific signaling pathways and promotes platelet activation and thrombosis. Platelet SR-BI, on the other hand, plays a critical role in the induction of platelet hyperreactivity and accelerated thrombosis under conditions associated with increased platelet cholesterol content. Intriguingly, oxidized high-density lipoprotein, an SR-BI ligand, can suppress platelet function. These recent findings demonstrate that platelet class B scavenger receptors play roles in thrombosis in dyslipidemia and may contribute to acute cardiovascular events in vivo in hypercholesterolemia.