The G protein‐coupled receptor ligand apelin‐13 ameliorates skeletal muscle atrophy induced by chronic kidney disease
Autor: | Yuki Enoki, Tomoya Nagai, Yuna Hamamura, Sumika Osa, Hideaki Nakamura, Kazuaki Taguchi, Hiroshi Watanabe, Toru Maruyama, Kazuaki Matsumoto |
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Jazyk: | angličtina |
Rok vydání: | 2023 |
Předmět: | |
Zdroj: | Journal of Cachexia, Sarcopenia and Muscle, Vol 14, Iss 1, Pp 553-564 (2023) |
Druh dokumentu: | article |
ISSN: | 2190-6009 2190-5991 |
DOI: | 10.1002/jcsm.13159 |
Popis: | Abstract Background Targeting of the apelin–apelin receptor (Apj) system may serve as a useful therapeutic intervention for the management of chronic kidney disease (CKD)‐induced skeletal muscle atrophy. We investigated the roles and efficacy of the apelin–Apj system in CKD‐induced skeletal muscle atrophy. Methods The 5/6‐nephrectomized mice were used as CKD models. AST‐120, a charcoal adsorbent of uraemic toxins (8 w/w% in diet), or apelin (1 μmol/kg) was administered to CKD mice to investigate the mechanism and therapeutic potential of apelin on CKD‐induced skeletal muscle atrophy. The effect of indoxyl sulfate, a uraemic toxin, or apelin on skeletal muscle atrophy was evaluated using mouse myoblast cells (C2C12 cells) in vitro. Results Skeletal muscle atrophy developed over time following nephrectomy at 12 weeks, as confirmed by a significant increase of atrogin‐1 and myostatin mRNA expression in the gastrocnemius (GA) muscle and a decrease of lower limb skeletal muscle weight (P |
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