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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

作者： Qin, Mengran 1 ; Wang, Yan 1 ; Wang, Zihan 5 ; Dong, Benchao 1 ; Yang, Peichuan 1 ; Liu, Youyi 1 ; Xi, Qianyun 4 ; Ma, Jianxiong 1 ;

作者机构： 1.Tianjin Univ, Tianjin Hosp, Tianjin 300211, Peoples R China

2.Tianjin Orthoped Inst, Tianjin 300050, Peoples R China

3.Tianjin Key Lab Orthoped Biomech & Med Engn, Tianjin 300050, Peoples R China

4.South China Agr Univ, Natl Engn Res Ctr Breeding Swine Ind, State Key Lab Livestock & Poultry Breeding, Coll Anim Sci,Guangdong Prov Key Lab Anim Nutr Reg, Guangzhou 510642, Guangdong, Peoples R China

5.Tianjin Agr Univ, Coll Anim Sci & Vet Med, Tianjin Key Lab Agr Anim Breeding & Hlth Husb, Tianjin 300392, Peoples R China

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

页码：

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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