心肌缺血/再灌注损伤中炎症反应作用机制的研究进展

被引：11

作者：

孟秋宏

王剑波

机构：

[1] 第四军医大学药学院药物研究所

来源：

临床内科杂志 | 2014年 / 31卷 / 03期

关键词：

心肌; 缺血再灌注; 炎症; 分子机制; 信号通路;

D O I：

暂无

中图分类号：

R541 [心脏疾病];

学科分类号：

100201 [内科学];

摘要：

<正>心肌缺血/再灌注(I/R)损伤是指心肌组织缺血后恢复血流.血液的再灌注不能使其功能恢复,反而加重其结构损伤和功能障碍的病理生理过程[1]。最终可能导致心肌梗塞、纤维化、心肌肥厚和心力衰竭。心肌L/R损伤的发生发展机制复杂。涉及到多系统多环节的异常,而炎症反应伴随其全过程,其中钙超载、活性氧(ROS)产生、中性粒细胞浸润和补体激活均参与调节心肌VR损伤的炎症反应[1]。因此,进一步了解炎症因子和相关信号通路在心肌VR损伤中的作用,对该病的防治具有十分重要的理论和应用价值。一、I/R损伤后心肌炎症相关的分子机制和信号通路

引用

页码：214 / 216

页数：3

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