骨骼肌损伤是最为常见的运动损伤之一，常因损伤肌肉难以良好修复，导致运动水平下降。目前认为，骨骼肌损伤组织中巨噬细胞由M1型向M2型极化对于骨骼肌修复至关重要；但是现有证据表明持续炎症刺激可能抑制了这一极化过程，从而造成肌肉再生障碍和继发纤维化，而其中的微环境调控机制有待阐明。我们在预实验中发现，受炎症因子刺激后的成肌细胞所产生外泌体可抑制M1型巨噬细胞向M2极化，进而初步证实外泌体可以介导miR-122和miR-206等microRNAs转移入巨噬细胞，并根据生物信息学分析推测其可能介导了巨噬细胞极化抑制。故我们计划进一步在体内外模型中，应用外泌体示踪技术，CRISPR/Cas9技术等，探究炎性微环境下成肌细胞释放的外泌体及其所转运的microRNA在巨噬细胞由M1型向M2型极化中的作用和机制，验证其对骨骼肌损伤后再生过程和纤维化水平的影响，为临床促进骨骼肌损伤后修复提供理论依据。

Skeletal muscle injury is one of the most common sports injuries. It often causes decline in sport ability due to inhibited repair of the injured muscle. Currently, it is believed that the polarization of macrophage from M1 type to M2 type in the injured skeletal muscle is critical to skeletal muscle repair. Yet, evidence indicated that continuous inflammation stimulation might have prohibited this polarization process, which subsequently resulted in deficient regeneration and subsequent fibrosis of muscle. The regulating mechanism behind this in the microenvironment remains unclear. Our preliminary studies discovered that, following the stimulation of inflammatory factors, myoblast-derived exosomes can prohibit M2 polarization of M1 macrophages, and that the exosomes can mediate the transfer of microRNAs, such as miR-122 and miR-206, into macrophages. Based on bioinformatics analysis, we then inferred that the exosomal miRNAs might have mediated the prohibition of macrophage polarization. As for the next step, with exosome tracing technique and CRISPR/Cas9 technique et al., we plan to investigate, in vitro and in vivo, the function and mechanism of myoblast-derived exosomes as well as the transported miRNAs on macrophage M1/M2 polarization under inflammatory microenvironment, and verify its influence on the skeletal muscle regeneration and fibrosis after injury, providing theoretical basis for clinical repair of injured skeletal muscle.