| First Author | Ozaki Y | Year | 2023 |
| Journal | Nat Commun | Volume | 14 |
| Issue | 1 | Pages | 4675 |
| PubMed ID | 37542026 | Mgi Jnum | J:355455 |
| Mgi Id | MGI:7517605 | Doi | 10.1038/s41467-023-40435-2 |
| Citation | Ozaki Y, et al. (2023) Myonectin protects against skeletal muscle dysfunction in male mice through activation of AMPK/PGC1alpha pathway. Nat Commun 14(1):4675 |
| abstractText | To maintain and restore skeletal muscle mass and function is essential for healthy aging. We have found that myonectin acts as a cardioprotective myokine. Here, we investigate the effect of myonectin on skeletal muscle atrophy in various male mouse models of muscle dysfunction. Disruption of myonectin exacerbates skeletal muscle atrophy in age-associated, sciatic denervation-induced or dexamethasone (DEX)-induced muscle atrophy models. Myonectin deficiency also contributes to exacerbated mitochondrial dysfunction and reduces expression of mitochondrial biogenesis-associated genes including PGC1alpha in denervated muscle. Myonectin supplementation attenuates denervation-induced muscle atrophy via activation of AMPK. Myonectin also reverses DEX-induced atrophy of cultured myotubes through the AMPK/PGC1alpha signaling. Furthermore, myonectin treatment suppresses muscle atrophy in senescence-accelerated mouse prone (SAMP) 8 mouse model of accelerated aging or mdx mouse model of Duchenne muscular dystrophy. These data indicate that myonectin can ameliorate skeletal muscle dysfunction through AMPK/PGC1alpha-dependent mechanisms, suggesting that myonectin could represent a therapeutic target of muscle atrophy. |
