Inflammation and its resolution as determinants of acute coronary syndromes.

Inflammation and its resolution as determinants of acute coronary syndromes.
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DOI:
10.1161/circresaha.114.302699
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发表时间:
2014-06-06
影响因子:
20.1
通讯作者:
Fisher EA
Fisher EA
中科院分区:
医学1区
文献类型:
--
作者:
Libby P;Tabas I;Fredman G;Fisher EA

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炎症导致急性冠状动脉综合征(ACS)发病机制中涉及的斑块的许多特征。此外,炎症通路不仅调节沉淀ACS的斑块的性质,而且还调节动脉粥样硬化血栓并发症的临床后果。该综合将提供关于控制ACS的炎症反应的基本机制的更新,并且还突出了促炎机制和可以促进炎症消退的内源性途径之间的持续平衡。对ACS相关炎症调节的抵消机制的认识丰富了我们对动脉粥样硬化这一重要表现的病理生理学的基本理解。此外,这些见解提供了潜在的新的治疗干预措施,以预防这种疾病的最终并发症的一瞥。
Inflammation contributes to many of the characteristics of plaques implicated in the pathogenesis of acute coronary syndromes (ACS). Moreover, inflammatory pathways not only regulate properties of plaques that precipitate ACS but also modulate the clinical consequences of the thrombotic complications of atherosclerosis. This synthesis will provide an update on the fundamental mechanisms of inflammatory responses that govern ACS, and also highlight the ongoing balance between pro-inflammatory mechanisms and endogenous pathways that can promote the resolution of inflammation. An appreciation of the countervailing mechanisms that modulate inflammation in relation to ACS enriches our fundamental understanding of the pathophysiology of this important manifestation of atherosclerosis. In addition, these insights furnish glimpses into potential novel therapeutic interventions to forestall this ultimate complication of the disease.