Inflammation in Myocardial Diseases

被引:379
作者
Marchant, David J. [1 ,2 ,3 ]
Boyd, John H. [1 ,2 ,4 ]
Lin, David C. [1 ,2 ,3 ]
Granville, David J. [1 ,2 ,3 ]
Garmaroudi, Farshid S. [1 ,2 ,3 ]
McManus, Bruce M. [1 ,2 ,3 ]
机构
[1] Univ British Columbia, James Hogg Res Ctr, Vancouver, BC V5Z 1M9, Canada
[2] Univ British Columbia, Inst Heart Lung Hlth, Vancouver, BC V5Z 1M9, Canada
[3] Univ British Columbia, Dept Pathol & Lab Med, Vancouver, BC V5Z 1M9, Canada
[4] Univ British Columbia, Dept Med, Vancouver, BC, Canada
基金
加拿大健康研究院;
关键词
inflammation; ischemia; infection; rejection; myocardium; TOLL-LIKE RECEPTOR; NF-KAPPA-B; NECROSIS-FACTOR-ALPHA; PROTEASE-ACTIVATED RECEPTORS; ISCHEMIA-REPERFUSION INJURY; CARDIAC ALLOGRAFT-REJECTION; NITRIC-OXIDE SYNTHASE; REGULATORY T-CELLS; COXSACKIEVIRUS-INDUCED MYOCARDITIS; LEFT-VENTRICULAR CONTRACTILITY;
D O I
10.1161/CIRCRESAHA.111.243170
中图分类号
R5 [内科学];
学科分类号
100201 [内科学];
摘要
Inflammatory processes underlie a broad spectrum of conditions that injure the heart muscle and cause both structural and functional deficits. In this article, we address current knowledge regarding 4 common forms of myocardial inflammation: myocardial ischemia and reperfusion, sepsis, viral myocarditis, and immune rejection. Each of these pathological states has its own unique features in pathogenesis and disease evolution, but all reflect inflammatory mechanisms that are partially shared. From the point of injury to the mobilization of innate and adaptive immune responses and inflammatory amplification, the cellular and soluble mediators and mechanisms examined in this review will be discussed with a view that both beneficial and adverse consequences arise in these human conditions. (Circ Res. 2012;110:126-144.)
引用
收藏
页码:126 / 144
页数:19
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