陆军军医大学缪洪明等研究人员合作，发现运动诱导的Musclin决定纤维脂肪生成前体细胞的命运来控制肌肉稳态。该项研究成果于2024年1月16日在线发表在《细胞—干细胞》上。

研究人员揭示了运动可降低纤维脂肪生成前体细胞（FAP）的频率，并通过Musclin减缓损伤或废用肌肉中胶原蛋白的沉积和脂肪的形成。从机理上讲，Musclin可通过上调FILIP1L抑制FAP的增殖并促进其凋亡。染色质免疫共沉淀（ChIP）-qPCR证实FoxO3a是FILIP1L的转录因子。此外，Musclin/FILIP1L 通路通过下调CD47的表达促进巨噬细胞吞噬凋亡的FAP。FILIP1L在FAP中的基因敲减会消除运动或Musclin对FAP的影响，以及对减少纤维化和脂肪浸润的益处。

总之，运动会在肌肉中形成肌细胞因子的微环境，并以依赖Musclin/FILIP1L的方式防止FAP的异常积累。施用外源性Musclin可产生治疗效果，是治疗肌肉萎缩或急性肌肉损伤的一种潜在方法。

据悉，运动对FAP的影响尚不清楚，直接的分子联系也尚不明确。

附：英文原文

Title: Exercise-induced Musclin determines the fate of fibro-adipogenic progenitors to control muscle homeostasis

Author: Xia Kang, Jin Qian, You-xing Shi, Xu-ting Bian, Li-dan Zhang, Gao-ming Li, Li-ting Wang, Jing Zhao, Zhen-yu Dong, Meng-meng Yang, Yu-Jia-Nan Chen, Kang-lai Tang, Hong-ming Miao

Issue&Volume: 2024-01-16

Abstract: The effects of exercise on fibro-adipogenic progenitors (FAPs) are unclear, and thedirect molecular link is still unknown. In this study, we reveal that exercise reducesthe frequency of FAPs and attenuates collagen deposition and adipose formation ininjured or disused muscles through Musclin. Mechanistically, Musclin inhibits FAPproliferation and promotes apoptosis in FAPs by upregulating FILIP1L. Chromatin immunoprecipitation(ChIP)-qPCR confirms that FoxO3a is the transcription factor of FILIP1L. In addition,the Musclin/FILIP1L pathway facilitates the phagocytosis of apoptotic FAPs by macrophagesthrough downregulating the expression of CD47. Genetic ablation of FILIP1L in FAPsabolishes the effects of exercise or Musclin on FAPs and the benefits on the reductionof fibrosis and fatty infiltration. Overall, exercise forms a microenvironment ofmyokines in muscle and prevents the abnormal accumulation of FAPs in a Musclin/FILIP1L-dependentmanner. The administration of exogenous Musclin exerts a therapeutic effect, demonstratinga potential therapeutic approach for muscle atrophy or acute muscle injury.

DOI: 10.1016/j.stem.2023.12.011

Source: https://www.cell.com/cell-stem-cell/fulltext/S1934-5909(23)00441-1