Pharmacological modulation of vascular inflammation in atherothrombosis
Pharmacological modulation of vascular inflammation in atherothrombosis
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DOI：
10.1111/j.1749-6632.2010.05784.x
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发表时间：
2010-01-01
期刊：
影响因子：
--
通讯作者：
Carluccio, Maria Annunziata
中科院分区：
文献类型：
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作者：
De Caterina, Raffaele;Massaro, Marika;Carluccio, Maria Annunziata
血管炎症，尤其是血管内皮细胞水平的炎症，已被证明在动脉粥样硬化的发生、发展和临床并发症中起着关键作用。炎症基因激活的共同分母似乎是一小部分转录因子，其中包括核因子-kappa B、激活蛋白-1(AP-1)和GATA-作为血管炎症的中心枢纽。抑制次级介质和主要触发因素(动脉粥样硬化危险因素)的策略似乎可以抑制动脉粥样硬化。然而，现在已经尝试解决血管炎症的中心枢纽。“旧的”药物，如潘生丁，现在也可以重新研究与抑制血管炎症有关的特性，可能是通过作用于共同的炎症中心。
Vascular inflammation, especially at the level of endothelial cells, has been shown to play a pivotal role in the inception, progression, and clinical complications of atherosclerosis. The common denominators for the activation of inflammatory genes appear to be a small subset of transcription factors-among which include nuclear factor-kappa B, activator protein-1 (AP-1), and GATA-that function as the central hub of vascular inflammation. Strategies directed to inhibit both the secondary mediators and the primary triggers (atherosclerosis risk factors) appear viable to inhibit atherosclerosis. However, attempts have now been made to address the central hub of vascular inflammation. "Old" drugs, such as dipyridamole, can also now be revisited for properties related to inhibition of vascular inflammation, probably by acting on the common hub of inflammation.