期刊
CURRENT PHARMACEUTICAL BIOTECHNOLOGY
卷 13, 期 1, 页码 77-87出版社
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/138920112798868700
关键词
Atherosclerosis; inflammation; innate immunity; toll-like receptors
资金
- British Heart Foundation
- European Commission [LSHM-CT-2006-037400]
- European Collaborative Project on Inflammation and Vascular Wall Remodelling in Atherosclerosis Acronym: AtheroRemo
- EU [HEALTH-2007-2.4.2-1. 2008]
- Graham-Dixon Charitable Trust
- Arthritis Research Campaign UK
Inflammation drives atherosclerosis. Toll-like receptor-2 and -4 are so far the strongest candidates for initiating innate immune signalling in atherosclerosis. Their signalling has implications for lesion development, foam cell formation, inflammation, matrix degradation and ischemia-reperfusion. The repertoire of TLR agonists is expanding. They collectively represent a conglomerate of structurally diverse molecular patterns requiring a high level of versatility in their sensing. Such versatility is achieved through cooperation of TLR heterodimers, co-receptors, and binding proteins. Several endogenous and exogenous molecular patterns engaging TLRs are associated with atherosclerosis development and complications. In this review, I describe how such molecular patterns are sensed, how they signal and what the consequences in the atherosclerotic plaque might be. The effect of TLR antagonising compounds in human and murine atherosclerosis is also addressed.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据