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MASP-2 的激活与人类缺血相关的坏死性心肌损伤有关。

MASP-2 activation is involved in ischemia-related necrotic myocardial injury in humans.

机构信息

Department of Anesthesiology, State University of New York Downstate Medical Center, Brooklyn, NY, USA.

出版信息

Int J Cardiol. 2013 Jun 20;166(2):499-504. doi: 10.1016/j.ijcard.2011.11.032. Epub 2011 Dec 15.

DOI:10.1016/j.ijcard.2011.11.032
PMID:22178059
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3310957/
Abstract

BACKGROUND/OBJECTIVES: Insufficient blood supply to the heart results in ischemic injury manifested clinically as myocardial infarction (MI). Following ischemia, inflammation is provoked and related to the clinical outcomes. A recent basic science study indicates that complement factor MASP-2 plays an important role in animal models of ischemia/reperfusion injury. We investigated the role of MASP-2 in human acute myocardial ischemia in two clinical settings: (1) Acute MI, and (2) Open heart surgery.

METHODS

A total of 187 human subjects were enrolled in this study, including 50 healthy individuals, 27 patients who were diagnosed of coronary artery disease (CAD) but without acute MI, 29 patients with acute MI referred for coronary angiography, and 81 cardiac surgery patients with surgically-induced global heart ischemia. Circulating MASP-2 levels were measured by ELISA.

RESULTS

MASP-2 levels in the peripheral circulation were significantly reduced in MI patients compared with those of healthy individuals or of CAD patients without acute MI. The hypothesis that MASP-2 was activated during acute myocardial ischemia was evaluated in cardiac patients undergoing surgically-induced global heart ischemia. MASP-2 was found to be significantly reduced in the coronary circulation of such patients, and the reduction of MASP-2 levels correlated independently with the increase of the myocardial necrosis marker, cardiac troponin I.

CONCLUSIONS

These results indicate an involvement of MASP-2 in ischemia-related necrotic myocardial injury in humans.

摘要

背景/目的：心肌的血液供应不足会导致缺血性损伤，临床上表现为心肌梗死（MI）。缺血后会引发炎症，与临床结局相关。最近的一项基础科学研究表明，补体因子 MASP-2 在缺血/再灌注损伤的动物模型中发挥重要作用。我们在两种临床情况下研究了 MASP-2 在人类急性心肌缺血中的作用：（1）急性 MI，（2）心脏直视手术。

方法

本研究共纳入 187 名受试者，包括 50 名健康个体、27 名被诊断为冠心病（CAD）但无急性 MI 的患者、29 名因急性 MI 而行冠状动脉造影的患者，以及 81 名因心脏直视手术导致的全心缺血的患者。通过 ELISA 法测定循环 MASP-2 水平。

结果

与健康个体或无急性 MI 的 CAD 患者相比，MI 患者外周循环中的 MASP-2 水平显著降低。我们在接受心脏直视手术导致的全心缺血的患者中评估了 MASP-2 在急性心肌缺血期间被激活的假说。结果发现，此类患者的冠状动脉循环中 MASP-2 明显减少，并且 MASP-2 水平的降低与心肌坏死标志物肌钙蛋白 I 的增加独立相关。

结论

这些结果表明 MASP-2 参与了人类与缺血相关的坏死性心肌损伤。

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