炎症免疫应答在心肌梗死后心脏重构中的作用

发布时间：2019-08-24 14:05

【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。
[Abstract]:The process of cardiac remodeling and repair after myocardial infarction can be divided into three stages. Inflammatory phase, fibroproliferation phase and stable phase, and inflammatory immune response plays an important role in this process. The initiation of early inflammatory response depends on the activation of innate immune system. Under the action of cytokines, chemokines and adhesion molecules, neutrophils, monocytes and other inflammatory cells gather to the heart, phagocytosis and degradation of necrotic cells and matrix fragments. Then the inflammatory reaction disappeared, and the inhibitory effect of inflammatory cells and cytokines was dominant, which promoted the differentiation and proliferation of fibroblasts and vascular endothelial cells, so that the necrotic site was repaired by fibrous tissue scar. It can be seen that the inflammatory immune process has a bidirectional regulatory effect on myocardial injury and repair after myocardial infarction. Excessive inflammatory reaction will lead to the increase of myocardial infarction area and aggravation of remodeling, while insufficient inflammatory response will affect the repair of myocardial tissue injury, while the aggravation of inflammatory response and fibrosis in non-infarction area is closely related to ventricular reverse remodeling. Therefore, it is of great clinical significance to regulate specific factors in the process of inflammatory response for different patients.
【作者单位】：上海交通大学医学院附属瑞金医院心血管内科;
【基金】：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)~~
【分类号】：R542.22

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