Myonectin protects against skeletal muscle dysfunction in male mice through activation of AMPK/PGC1α pathway

Yuta Ozaki, Koji Ohashi (), Naoya Otaka, Hiroshi Kawanishi, Tomonobu Takikawa, Lixin Fang, Kunihiko Takahara, Minako Tatsumi, Sohta Ishihama, Mikito Takefuji, Katsuhiro Kato, Yuuki Shimizu, Yasuko K. Bando, Aiko Inoue, Masafumi Kuzuya, Shinji Miura, Toyoaki Murohara and Noriyuki Ouchi ()
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Yuta Ozaki: Nagoya University Graduate School of Medicine
Koji Ohashi: Nagoya University Graduate School of Medicine
Naoya Otaka: Nagoya University Graduate School of Medicine
Hiroshi Kawanishi: Nagoya University Graduate School of Medicine
Tomonobu Takikawa: Nagoya University Graduate School of Medicine
Lixin Fang: Nagoya University Graduate School of Medicine
Kunihiko Takahara: Nagoya University Graduate School of Medicine
Minako Tatsumi: Nagoya University Graduate School of Medicine
Sohta Ishihama: Nagoya University Graduate School of Medicine
Mikito Takefuji: Nagoya University Graduate School of Medicine
Katsuhiro Kato: Nagoya University Graduate School of Medicine
Yuuki Shimizu: Nagoya University Graduate School of Medicine
Yasuko K. Bando: Nagoya University Graduate School of Medicine
Aiko Inoue: Nagoya University Graduate School of Medicine
Masafumi Kuzuya: Nagoya University Graduate School of Medicine
Shinji Miura: University of Shizuoka
Toyoaki Murohara: Nagoya University Graduate School of Medicine
Noriyuki Ouchi: Nagoya University Graduate School of Medicine

Nature Communications, 2023, vol. 14, issue 1, 1-17

Abstract: Abstract 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 PGC1α 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/PGC1α 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/PGC1α-dependent mechanisms, suggesting that myonectin could represent a therapeutic target of muscle atrophy.

Date: 2023
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DOI: 10.1038/s41467-023-40435-2

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