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首页> 外文期刊>The journal of clinical investigation >Annexin A1 drives macrophage skewing to accelerate muscle regeneration through AMPK activation
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Annexin A1 drives macrophage skewing to accelerate muscle regeneration through AMPK activation

机译：Annexin A1驱动巨噬细胞偏斜以通过AMPK激活加速肌肉再生

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Understanding the circuits that promote an efficient resolution of inflammation is crucial to deciphering the molecular and cellular processes required to promote tissue repair. Macrophages play a central role in the regulation of inflammation, resolution, and repair/regeneration. Using a model of skeletal muscle injury and repair, herein we identified annexin A1 (AnxA1) as the extracellular trigger of macrophage skewing toward a pro-reparative phenotype. Brought into the injured tissue initially by migrated neutrophils, and then overexpressed in infiltrating macrophages, AnxA1 activated FPR2/ALX receptors and the downstream AMPK signaling cascade, leading to macrophage skewing, dampening of inflammation, and regeneration of muscle fibers. Mice lacking AnxA1 in all cells or only in myeloid cells displayed a defect in this reparative process. In vitro experiments recapitulated these properties, with AMPK-null macrophages lacking AnxA1-mediated polarization. Collectively, these data identified the AnxA1/FPR2/AMPK axis as an important pathway in skeletal muscle injury regeneration.
机译：了解促进促进炎症的有效分离的电路对于破译促进组织修复所需的分子和细胞工艺至关重要。巨噬细胞在调节炎症，分辨率和修复/再生的调节中起着核心作用。使用骨骼肌损伤和修复模型，在本文中，我们鉴定了Annexin A1（ANXA1）作为巨噬细胞偏向于重新计量表型的巨噬细胞触发。最初通过迁移的中性粒细胞引入受损的组织，然后在浸润的巨噬细胞中过表达，ANXA1激活的FPR2 / ALX受体和下游AMPK信号传导级联，导致巨噬细胞倾斜，炎症的抑制和肌肉纤维的再生。在所有细胞中缺乏ANXA1或仅在骨髓细胞中缺乏ANXA1的小鼠在该重复过程中显示出缺陷。体外实验综合，缺乏ANXA1介导的极化的AMPK-NULL巨噬细胞。总的来说，这些数据将ANXA1 / FPR2 / AMPK轴鉴定为骨骼肌损伤再生中的重要途径。

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