Interleukin-1 Beta as a Target for Atherosclerosis Therapy: Biological Basis of CANTOS and Beyond.
Interleukin-1 Beta as a Target for Atherosclerosis Therapy: Biological Basis of CANTOS and Beyond.
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DOI：
10.1016/j.jacc.2017.09.028
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发表时间：
2017-10-31
影响因子：
24
通讯作者：
Libby P
中科院分区：
文献类型：
--
作者：
Libby P
炎症途径推动动脉粥样硬化的形成，并将传统的危险因素与动脉粥样硬化及其并发症联系起来。一种炎症介质作为心血管疾病的治疗靶点脱颖而出。本文综述的实验和临床证据支持白介素1β(IL-1β)在这方面是局部的血管和全身的贡献者。固有的血管壁细胞和皮损白细胞都可以产生这种细胞因子。斑块中的局部刺激有助于通过称为炎症体的分子集合的作用产生活性的IL-1β。干扰IL-1作用的临床适用的干预措施可以改善心血管结果，开创了动脉粥样硬化抗炎治疗的新时代。这里描述的转换路径说明了基础血管生物学的进步如何改变治疗。生物标记物导向的抗炎干预应用有望帮助我们为心血管患者实现更精确和个性化的治疗分配。
Inflammatory pathways drive atherogenesis and link traditional risk factors to atherosclerosis and its complications. One inflammatory mediator has come to the fore as a therapeutic target in cardiovascular disease. The experimental and clinical evidence reviewed here support interleukin-1 beta (IL-1β) as both a local vascular and systemic contributor in this regard. Intrinsic vascular wall cells and lesional leukocytes alike can produce this cytokine. Local stimuli in the plaque favor the generation of active IL-1β through the action of a molecular assembly known as the inflammasome. Clinically applicable interventions that interfere with IL-1 action can improve cardiovascular outcomes, ushering in a new era of anti-inflammatory therapies for atherosclerosis. The translational path described here illustrates how advances in basic vascular biology may transform therapy. Biomarker-directed application of anti-inflammatory interventions promises to help us achieve a more precise and personalized allocation of therapy for our cardiovascular patients.
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影响因子：
37.8
作者：
Cook NR;Paynter NP;Eaton CB;Manson JE;Martin LW;Robinson JG;Rossouw JE;Wassertheil-Smoller S;Ridker PM
通讯作者：
Ridker PM
影响因子：
20.1
作者：
GALIS, ZS;MUSZYNSKI, M;LIBBY, P
通讯作者：
LIBBY, P
影响因子：
6.8
作者：
Abbate, Antonio;Van Tassell, Benjamin W.;Biondi-Zoccai, Giuseppe G. L.
通讯作者：
Biondi-Zoccai, Giuseppe G. L.
影响因子：
9.2
作者：
Dinarello, Charles A.
通讯作者：
Dinarello, Charles A.
影响因子：
15.9
作者：
Alexander, Matthew R.;Moehle, Christopher W.;Owens, Gary K.
通讯作者：
Owens, Gary K.