Department of Medical Biochemistry, Academic Medical Center, University of Amsterdam, The Netherlands.
Curr Atheroscler Rep. 2012 Jun;14(3):254-63. doi: 10.1007/s11883-012-0240-5.
Recent years have seen a tremendous development of our insight into the biology of atherosclerosis and its acute thrombotic manifestations. Inflammation now takes center stage among traditional risk factors as a decisive factor in cardiovascular risk. Consequently, its assessment and modulation have become key to clinical care and fundamental research alike. Plaque macrophages orchestrate many of the inflammatory processes that occur throughout atherogenesis. These cells are characteristically heterogeneous and adopt diverse activation states in response to micro-environmental triggers. In this review, macrophage-mediated inflammation in atherosclerosis sets the scene for a discussion of the gene regulatory mechanisms that facilitate and shape polarized macrophage phenotypes. When applicable, we consider these factors within the context of atherosclerosis and reflect on opportunities for future application.
近年来,我们对动脉粥样硬化生物学及其急性血栓形成表现的认识有了巨大的发展。炎症现在取代了传统的危险因素,成为心血管风险的决定性因素。因此,它的评估和调节已经成为临床护理和基础研究的关键。斑块内的巨噬细胞协调了动脉粥样硬化发生过程中发生的许多炎症过程。这些细胞具有特征性的异质性,并对微环境触发因素表现出不同的激活状态。在这篇综述中,动脉粥样硬化中巨噬细胞介导的炎症为讨论促进和塑造极化巨噬细胞表型的基因调控机制奠定了基础。在适用的情况下,我们将这些因素置于动脉粥样硬化的背景下进行考虑,并探讨未来应用的机会。