动脉粥样硬化
发病机制
细胞生物学
清道夫受体
巨噬细胞
趋化因子
生物
纤维帽
表型
脂蛋白
泡沫电池
免疫学
医学
炎症
胆固醇
病理
体外
内分泌学
内科学
基因
生物化学
作者
Bennett G. Childs,Darren J. Baker,Tobias Wijshake,Cheryl A. Conover,Judith Campisi,Jan M. van Deursen
出处
期刊:Science
[American Association for the Advancement of Science]
日期:2016-10-27
卷期号:354 (6311): 472-477
被引量:928
标识
DOI:10.1126/science.aaf6659
摘要
Wreaking havoc while (growth-)arrested Cells enter a state of senescence in response to certain stresses. Studying mouse models, Childs et al. examined the role of senescent lipid-loaded macrophages (so-called “foam cells”) in the pathogenesis of atherosclerosis. At early stages of atherosclerosis, senescent foam cells promoted the expression of inflammatory cytokines. At later stages, they promoted the expression of matrix metalloproteases implicated in the rupture of atherosclerotic plaque, which can lead to blood clots. Experimental removal of the senescent cells had beneficial effects at both stages of the disease. Science , this issue p. 472
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