Adipose-derived exosomes ameliorate skeletal muscle atrophy via miR-146a-5p/IGF-1R signaling

文献类型： 外文期刊

第一作者： Qin, Mengran

作者： Qin, Mengran;Zhu, Jiahao;Xing, Lipeng;Fan, Yaotian;Luo, Junyi;Sun, Jiajie;Chen, Ting;Zhang, Yongliang;Xi, Qianyun;Qin, Mengran;Qin, Mengran

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关键词： Muscle atrophy; IGF-1R; Exosomes; miR-146a-5p; Skeletal muscle; Adipose

期刊名称：JOURNAL OF NANOBIOTECHNOLOGY （ 影响因子：12.6； 五年影响因子：12.3 ）

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年卷期： 2024 年 22 卷 1 期

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收录情况： SCI

摘要： The study of muscle disorders has gained popularity, with a particular emphasis on the relationship between adipose tissue and skeletal muscle. In our investigation, we discovered that the deletion of miR-146a-5p specifically in adipose tissue (aKO) led to a notable rise in mice's mass and adiposity. In contrast, it led to a decline in lean mass, ability to exercise, diameter of muscle fibers, and the levels of genes associated with differentiation. The co-culture experiment showed that the transfection of miR-146a-5p mimics to 3T3-L1 significantly suppressive cell growth and promotes myotube differentiation in C2C12 cells. Exosomes from white adipose tissue (WAT) of aKO mice (aKO-WAT-Exos) significantly promoted muscle atrophy and inhibited differentiation of C2C12 cells but were reversed by co-incubation with miR-146a-5p-mimics. The miR-146a-5p can specifically target IGF-1R to improve skeletal muscle wasting. In this process, the PI3K/AKT/mTOR pathway is activated or the FoxO3 pathway is inhibited to enhance the synthesis of skeletal muscle proteins. Significantly, miR-146a-5p serves a crucial function as a microRNA in the communication of the fat-muscle connection. It can be transported through the pathway of exosomes derived from adipose tissue, ultimately ameliorating skeletal muscle atrophy and modulating body mass index (BMI).

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