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炎症在动脉粥样硬化中的生物学作用。

The biological role of inflammation in atherosclerosis.

机构信息

UBC James Hogg Research Centre, Institute for Heart and Lung Health, St Paul's Hospital, University of British Columbia, Vancouver, BC, Canada.

出版信息

Can J Cardiol. 2012 Nov-Dec;28(6):631-41. doi: 10.1016/j.cjca.2012.06.023. Epub 2012 Sep 15.

DOI:10.1016/j.cjca.2012.06.023
PMID:22985787
Abstract

The concept of the involvement of inflammation in the pathogenesis of atherosclerosis has existed since the 1800s, stemming from sentinel pathologic observations made by Rudolf Virchow, Karl Rokitansky, and others. Our understanding of the complex role played by immune and inflammatory mediators in the initiation and progression of atherosclerosis has evolved considerably in the intervening years, and today, a dramatically evolved understanding of these processes has led to advances in both diagnostic and prognostic approaches, as well as novel treatment modalities targeting inflammatory and immune mediators. Therapeutic interventions working through multiple mechanisms involved in atheroma pathogenesis, such as statins, which both lower lipids and alter the inflammatory milieu in the vessel wall, hold promise for the future. In this brief review, we explore the biological role of inflammation in atherosclerosis, with a focus on cellular involvement in both acute and chronic inflammation, and outline novel biomarkers of inflammation and atherosclerosis with a particular focus on the potential application of these novel approaches in improving strategies for disease diagnosis and management.

摘要

自 19 世纪以来,炎症在动脉粥样硬化发病机制中的作用的概念就已经存在,这源于 Rudolf Virchow、Karl Rokitansky 等人的开创性病理观察。在这期间,我们对免疫和炎症介质在动脉粥样硬化的发生和进展中所起的复杂作用的理解有了相当大的发展,如今,对这些过程的理解有了显著的提高,这也为诊断和预后方法的改进以及针对炎症和免疫介质的新型治疗方式带来了新的契机。通过他汀类药物等多种机制作用于动脉粥样硬化发病机制的治疗干预措施,既降低了血脂,又改变了血管壁中的炎症环境,为未来带来了希望。在这篇简短的综述中,我们探讨了炎症在动脉粥样硬化中的生物学作用,重点关注了急性和慢性炎症中细胞的参与,并概述了炎症和动脉粥样硬化的新型生物标志物,特别关注了这些新方法在改善疾病诊断和管理策略方面的潜在应用。

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