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白三烯信号通路在动脉粥样硬化和局部缺血中的作用

Leukotriene signaling in atherosclerosis and ischemia.

作者信息

Bäck Magnus

机构信息

INSERM U698, Bichat Hospital, 46 rue Henri Huchard, 75018, Paris, France.

出版信息

Cardiovasc Drugs Ther. 2009 Feb;23(1):41-8. doi: 10.1007/s10557-008-6140-9. Epub 2008 Oct 24.

DOI:10.1007/s10557-008-6140-9
PMID:18949546
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2663527/
Abstract

INTRODUCTION

The inflammatory process of atherosclerosis is associated with several pathophysiological reactions within the vascular wall. The arachidonic acid released by phospholipase A(2) serves as substrate for the production of a group of lipid mediators known as the leukotrienes, which induce pro-inflammatory signaling through activation of specific BLT and CysLT receptors.

DISCUSSION

Leukotriene signaling has been implicated in early lipid retention and foam cell accumulation, as well as in the development of intimal hyperplasia and advanced atherosclerotic lesions. Furthermore, the association of leukotrienes with degradation of extracellular matrix has suggested a role in atherosclerotic plaque rupture. Finally, studies of either myocardial or cerebral ischemia and reperfusion indicate that leukotriene signaling in addition may be involved in the development of ischemic injury.

CONCLUSION

Both leukotriene synthesis inhibitors and leukotriene receptor antagonists have been suggested to induce beneficial effects at different stages of the atherosclerosis process.

摘要

引言

动脉粥样硬化的炎症过程与血管壁内的多种病理生理反应相关。磷脂酶A(2)释放的花生四烯酸作为一组称为白三烯的脂质介质产生的底物,这些白三烯通过激活特定的BLT和半胱氨酰白三烯受体诱导促炎信号。

讨论

白三烯信号传导与早期脂质潴留和泡沫细胞积聚有关,也与内膜增生和晚期动脉粥样硬化病变的发展有关。此外,白三烯与细胞外基质降解的关联表明其在动脉粥样硬化斑块破裂中起作用。最后,心肌或脑缺血及再灌注的研究表明,白三烯信号传导还可能参与缺血性损伤的发展。

结论

白三烯合成抑制剂和白三烯受体拮抗剂均被认为在动脉粥样硬化过程的不同阶段具有有益作用。

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本文引用的文献

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Curr Atheroscler Rep. 2008 Jun;10(3):244-51. doi: 10.1007/s11883-008-0038-7.
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Fenofibrate reduces lipoprotein associated phospholipase A2 mass and oxidative lipids in hypertriglyceridemic subjects with the metabolic syndrome.非诺贝特可降低患有代谢综合征的高甘油三酯血症患者的脂蛋白相关磷脂酶A2水平和氧化脂质。
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