传出细胞增多
CD47型
吞噬作用
细胞凋亡
炎症
疾病
程序性细胞死亡
免疫学
抗体
间隙
下调和上调
生物
医学
巨噬细胞
癌症研究
病理
体外
生物化学
泌尿科
基因
作者
Yoko Kojima,Jens-Peter Volkmer,Kelly M. McKenna,Mete Civelek,Aldons J. Lusis,Clint L. Miller,Daniel DiRenzo,Vivek Nanda,Jianqin Ye,Andrew J. Connolly,Eric E. Schadt,Thomas Quertermous,Paola Betancur,Lars Mäegdefessel,Ljubica Matic,Ulf Hedin,Irving L. Weissman,Nicholas J. Leeper
出处
期刊:Nature
[Nature Portfolio]
日期:2016-07-19
卷期号:536 (7614): 86-90
被引量:547
摘要
Atherosclerosis is the disease process that underlies heart attack and stroke. Advanced lesions at risk of rupture are characterized by the pathological accumulation of diseased vascular cells and apoptotic cellular debris. Why these cells are not cleared remains unknown. Here we show that atherogenesis is associated with upregulation of CD47, a key anti-phagocytic molecule that is known to render malignant cells resistant to programmed cell removal, or 'efferocytosis'. We find that administration of CD47-blocking antibodies reverses this defect in efferocytosis, normalizes the clearance of diseased vascular tissue, and ameliorates atherosclerosis in multiple mouse models. Mechanistic studies implicate the pro-atherosclerotic factor TNF-α as a fundamental driver of impaired programmed cell removal, explaining why this process is compromised in vascular disease. Similar to recent observations in cancer, impaired efferocytosis appears to play a pathogenic role in cardiovascular disease, but is not a fixed defect and may represent a novel therapeutic target.
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