上海交通大学学报（医学版）

上海交通大学学报（医学版） ›› 2017, Vol. 37 ›› Issue (6): 830-.doi: 10.3969/j.issn.1674-8115.2017.06.020

• 论著（临床研究） • 上一篇    下一篇

炎症免疫应答在心肌梗死后心脏重构中的作用

范骎，陶蓉   

  1. 上海交通大学 医学院附属瑞金医院心血管内科，上海 200025
  • 出版日期:2017-06-28 发布日期:2017-07-05
  • 作者简介:?范骎（1990—），女，博士生；电子信箱 : fanqin125@163.com
  • 基金资助:

    国家自然科学基金（81370256，81670352）；上海市教育委员会高峰高原学科建设计划（20152205）

Inflammatory response in cardiac remodeling after myocardial infarction

FAN Qin, TAO Rong   

  1. Department of Cardiology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China
  • Online:2017-06-28 Published:2017-07-05
  • Supported by:

    National Natural Science Foundation of China, 81370256, 81670352; Shanghai Municipal Education Commission—Gaofeng Clinical Medicine Grant Support, 20152205

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摘要：

心肌梗死后的心脏重构与修复过程可分为 3 个阶段。炎症期、纤维增殖期及稳定期，而炎症免疫应答在这一过程中发挥了重 要作用。早期炎症反应的启动依赖固有免疫系统的激活，在细胞因子、趋化因子及黏附分子的作用下，中性粒细胞、单核巨噬细胞等 炎症细胞向心脏集聚，吞噬降解坏死细胞及基质碎片。随后炎症反应消退，抑炎性细胞及细胞因子的作用占优势，促进成纤维细胞和 血管内皮细胞分化增殖，从而使坏死部位被纤维组织瘢痕修复。由此可见，炎症免疫过程对于心肌梗死后心肌的损伤与修复具有双向 调节作用。炎症反应过度会导致心肌梗死面积增大、重构加重，炎症反应不足则会影响心肌组织的损伤修复，而非梗死区炎症反应及 纤维化的加重则与心室逆重构密切相关。因此，针对不同患者，对炎症反应过程中的特定因子进行特异性调节具有重要的临床意义。

关键词: 心肌梗死, 心脏重构, 炎症, 免疫反应

Abstract:

The remodeling and reparative process post myocardial infarction (MI) can be divided into three phases: the inflammatory phase, the proliferative phase and the stable phase. The inflammatory immune response plays an important part in the process of cardiac remodeling. First of all, the initiation of inflammatory response relies on the activation of innate immunity with a group of pro-inflammatory cytokines, chemokines and adhesion molecules. These molecules lead to the infiltration of the infarct area with neutrophils and mononuclear cells, further clearing the wound from dead cardiomyocytes and matrix debris. After resolution of inflammatory response, reparative cells and cytokines infiltrate into the heart and promote the differentiation and growth of myofibroblasts and endothelial cells, contributing to wound contraction as well as producing fiber tissue to form a scar. Moreover, overactive immune responses could accentuate infarct injury and dilative remodeling while deficiency of inflammation leads to insufficient repair, which highlights the dual function of the immune response in myocardial injury and repair post MI. Also the intense immune response along with fibrosis in non-infarct area is also closely associated with adverse remodeling. Thus, targeting specific factors in the inflammatory reaction may hold promise in patients with MI.

Key words: myocardial infarction, cardiac remodeling, inflammation, immune response