C-reactive protein and complement are important mediators of tissue damage in acute myocardial infarction.
C-reactive protein and complement are important mediators of tissue damage in acute myocardial infarction.
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DOI：
10.1084/jem.190.12.1733
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发表时间：
1999-12-20
期刊：
影响因子：
--
通讯作者：
Pepys MB
中科院分区：
文献类型：
--
作者：
Griselli M;Herbert J;Hutchinson WL;Taylor KM;Sohail M;Krausz T;Pepys MB
人类心肌梗塞会引发急性期反应，C 反应蛋白 (CRP)（经典的急性期血浆蛋白）与补体一起沉积在梗塞灶内。血浆 CRP 峰值与梗死后发病率和死亡率密切相关。人类 CRP 与受损细胞结合并激活补体，但大鼠 CRP 不会激活补体。在这里，我们发现，结扎冠状动脉后向大鼠注射人 CRP 可重复地将梗死面积扩大约 40%。眼镜蛇毒因子产生的体内补体耗竭完全消除了这种作用。即使在冠状动脉结扎后 2 小时内开始补体耗竭，也能显着减少梗塞面积。这些观察结果表明，人类 CRP 和补体激活是缺血性心肌损伤的主要介质，并将它们确定为冠心病的治疗靶点。
Myocardial infarction in humans provokes an acute phase response, and C-reactive protein (CRP), the classical acute phase plasma protein, is deposited together with complement within the infarct. The peak plasma CRP value is strongly associated with postinfarct morbidity and mortality. Human CRP binds to damaged cells and activates complement, but rat CRP does not activate complement. Here we show that injection of human CRP into rats after ligation of the coronary artery reproducibly enhanced infarct size by ∼40%. In vivo complement depletion, produced by cobra venom factor, completely abrogated this effect. Complement depletion also markedly reduced infarct size, even when initiated up to 2 h after coronary ligation. These observations demonstrate that human CRP and complement activation are major mediators of ischemic myocardial injury and identify them as therapeutic targets in coronary heart disease.