Adipose-derived small extracellular vesicle miR-146a-5p targets Fbx32 to regulate mitochondrial autophagy and delay aging in skeletal muscle

文献类型： 外文期刊

第一作者： Qin, Mengran

作者： Qin, Mengran;Wang, Yan;Dong, Benchao;Yang, Peichuan;Liu, Youyi;Ma, Jianxiong;Qin, Mengran;Wang, Yan;Dong, Benchao;Yang, Peichuan;Liu, Youyi;Ma, Jianxiong;Qin, Mengran;Wang, Yan;Dong, Benchao;Yang, Peichuan;Liu, Youyi;Ma, Jianxiong;Qin, Mengran;Xi, Qianyun;Wang, Zihan;Liu, Youyi

作者机构：

关键词： sEV; miR-146a-5p; Fbx32; Mitochondrial autophagy; Aging

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

ISSN：

年卷期： 2025 年 23 卷 1 期

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收录情况： SCI

摘要： This study investigates how miR-146a-5p, found in adipose tissue-derived small extracellular vesicles (sEV), influences mitochondrial autophagy and its impact on delaying skeletal muscle aging through the targeting of Fbx32. The findings highlight miR-146a-5p as crucial in skeletal muscle development and aging, influencing autophagy, apoptosis, differentiation, and proliferation, collectively impacting muscle atrophy. In C2C12 cells, miR-146a-5p mimics decreased apoptosis, autophagy, and reactive oxygen species (ROS) levels, while enhancing ATP production; conversely, miR-146a-5p inhibitors had the opposite effects. Furthermore, miR-146a-5p-enriched sEV from adipose tissue alleviated skeletal muscle atrophy in aged mice and promoted muscle fiber growth and repair by regulating mitochondrial autophagy and apoptosis. Mechanistically, miR-146a-5p modulated mitochondrial autophagy in myoblasts by targeting Fbx32 and impacting the FoxO3 signaling pathway. This led to a notable decrease in apoptosis-related gene expression, reduced ROS production, and elevated ATP levels. In conclusion, miR-146a-5p derived from WAT-sEV modulates myoblast autophagy, apoptosis, ROS, and differentiation through the Fbx32/FoxO3 signaling axis. This work presents a novel molecular target and theoretical framework for delaying skeletal muscle aging and developing therapies for skeletal muscle-related disorders.

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