固有免疫相关模式识别受体（PRRs）介导的炎症免疫反应参与心肌缺血再灌注（IR）损伤。我们发现，心肌IR损伤早期心脏巨噬细胞特异性高表达PRR成员Dectin-2，促进其表达M1巨噬细胞相关炎症因子和中性粒细胞趋化因子，进而促进中性粒细胞向心脏聚集，共同介导IR损伤。进一步研究证实，miR-26a负调控巨噬细胞Dectin-2介导的免疫炎症反应参与抑制心肌IR损伤，且miR-26a转基因小鼠IR后心梗面积和心功能较野生型小鼠均有显著改善，提示miR-26a靶向Dectin-2调控心肌IR后巨噬细胞炎症免疫反应。后续实验将探讨：心肌IR后miR-26a在心脏的表达谱；心肌IR后促炎因子调控miR-26a的分子机制；巨噬细胞miR-26a在心肌IR损伤中的作用； miR-26a靶向Dectin-2调控巨噬细胞极化和炎症因子表达的机制；从临床角度阐明miR-26a与急性心肌梗死的相关性。

Immuno-inflammatory responses induced by pattern recognition receptors (PRRs) are closely involved in the process of myocardial Ischemia/Reperfusion (IR) injury. The present study indicated that Dectin-2, a major C-type lectin-like receptors of the PRRs, was highly induced in cardiac macrophages at the early stage of myocardial IR injury. Activation of Dectin-2 promoted the expression of M1 macrophage-related cytokines and neutrophil chemotactic factors, leading to the excess infiltration of neutrophils into the heart and subsequent deterioration. Results from gene microarray, target prediction and cell transfection implied that miR-26a participated in inhibiting myocardial IR injury through the negative regulation of inflammation induced by macrophage Dectin-2. In addition, miR-26a transgenic mice enjoyed less infarct size and better cardiac function after myocardial IR injury compared with wide-type ones. In the future study, we will investigate the expression profile of miR-26a in post-IR heart, the mechanisms of regulating miR-26a by NF-κB, the involvement of macrophage miR-26a in myocardial IR injury, the mechanisms of miR-26a/Dectin-2 pathway during the regulation of macrophage polarization and cytokine expression and the clinical correlation between miR-26a and acute myocardial infarction.