Academic Journal
Adipose-derived exosomes ameliorate skeletal muscle atrophy via miR-146a-5p/IGF-1R signaling.
| العنوان: | Adipose-derived exosomes ameliorate skeletal muscle atrophy via miR-146a-5p/IGF-1R signaling. |
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| المؤلفون: | Qin, Mengran, Zhu, Jiahao, Xing, Lipeng, Fan, Yaotian, Luo, Junyi, Sun, Jiajie, Chen, Ting, Zhang, Yongliang, Xi, Qianyun |
| المصدر: | J Nanobiotechnology ; ISSN:1477-3155 ; Volume:22 ; Issue:1 |
| بيانات النشر: | BioMed Central |
| سنة النشر: | 2024 |
| المجموعة: | PubMed Central (PMC) |
| مصطلحات موضوعية: | Adipose, Exosomes, IGF-1R, Muscle atrophy, Skeletal muscle, miR-146a-5p |
| الوصف: | 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). |
| نوع الوثيقة: | article in journal/newspaper |
| اللغة: | English |
| Relation: | https://doi.org/10.1186/s12951-024-02983-7; https://pubmed.ncbi.nlm.nih.gov/39696303; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11657514/ |
| DOI: | 10.1186/s12951-024-02983-7 |
| الاتاحة: | https://doi.org/10.1186/s12951-024-02983-7 https://pubmed.ncbi.nlm.nih.gov/39696303 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11657514/ |
| Rights: | © 2024. The Author(s). |
| رقم الانضمام: | edsbas.3F6B1E67 |
| قاعدة البيانات: | BASE |
| DOI: | 10.1186/s12951-024-02983-7 |
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