【摘要】：心肌梗死后的心臟重構(gòu)與修復過程可分為3個階段。炎癥期、纖維增殖期及穩(wěn)定期,而炎癥免疫應答在這一過程中發(fā)揮了重要作用。早期炎癥反應的啟動依賴固有免疫系統(tǒng)的激活,在細胞因子、趨化因子及黏附分子的作用下,中性粒細胞、單核巨噬細胞等炎癥細胞向心臟集聚,吞噬降解壞死細胞及基質(zhì)碎片。隨后炎癥反應消退,抑炎性細胞及細胞因子的作用占優(yōu)勢,促進成纖維細胞和血管內(nèi)皮細胞分化增殖,從而使壞死部位被纖維組織瘢痕修復。由此可見,炎癥免疫過程對于心肌梗死后心肌的損傷與修復具有雙向調(diào)節(jié)作用。炎癥反應過度會導致心肌梗死面積增大、重構(gòu)加重,炎癥反應不足則會影響心肌組織的損傷修復,而非梗死區(qū)炎癥反應及纖維化的加重則與心室逆重構(gòu)密切相關(guān)。因此,針對不同患者,對炎癥反應過程中的特定因子進行特異性調(diào)節(jié)具有重要的臨床意義。
[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.
【作者單位】： 上海交通大學醫(yī)學院附屬瑞金醫(yī)院心血管內(nèi)科;
【基金】：國家自然科學基金(81370256,81670352) 上海市教育委員會高峰高原學科建設(shè)計劃(20152205)~~
【分類號】：R542.22

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