Inflammatory Response During Myocardial Infarction

被引:32
|
作者
Oliveira, Joaquim B. [1 ]
Soares, Alexandre A. S. M. [1 ]
Sposito, Andrei C. [1 ]
机构
[1] Univ Estadual Campinas, Lab Atherosclerosis & Vasc Biol, Campinas, Brazil
来源
关键词
NF-KAPPA-B; GLYCATION END-PRODUCTS; LEFT-VENTRICULAR DYSFUNCTION; ANTI-C5 COMPLEMENT ANTIBODY; NECROSIS-FACTOR-ALPHA; MOBILITY GROUP BOX-1; NUCLEAR-PROTEIN HMGB1; INNATE IMMUNE-SYSTEM; TOLL-LIKE RECEPTOR-2; NLRP3; INFLAMMASOME;
D O I
10.1016/bs.acc.2017.12.002
中图分类号
R446 [实验室诊断]; R-33 [实验医学、医学实验];
学科分类号
1001 ;
摘要
The occlusion of a coronary artery by a thrombus generated on a ruptured atherosclerotic plaque has been pursued in the last decades as a determining event for the clinical outcome after myocardial infarction (MI). Yet, MI causes a cell death wave front, which triggers an inflammatory response to clear cellular debris, and which in excess can double the myocardial lesion and influence the clinical prognosis in the short and long term. Accordingly, proper, timely regulated inflammatory response has now been considered a second pivotal player in cardiac recovery after MI justifying the search for pharmacological strategies to modulate inflammatory effectors. This chapter reviews the key events and the main effectors of inflammation after myocardial ischemic insult, as well as the contribution of this phenomenon to the progression of atherosclerosis.
引用
收藏
页码:39 / 79
页数:41
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