TRIM16 facilitates SIRT‐1‐dependent regulation of antioxidant response to alleviate age‐related sarcopenia

Background Age‐related sarcopenia, characterized by reduced skeletal muscle mass and function, significantly affects the health of the elderly individuals. Oxidative stress plays a crucial role in the development of sarcopenia. Tripartite motif containing 16 (TRIM16) is implicated in orchestrating a...

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Published in:Journal of cachexia, sarcopenia and muscle sarcopenia and muscle, 2024-10, Vol.15 (5), p.2056-2070
Main Authors: Guo, Ai, Huang, Ke, Lu, Quanyi, Tao, Bailong, Li, Kai, Jiang, Dianming
Format: Article
Language:English
Subjects:
Antibodies
Antioxidants
Biotechnology
Body composition
Cell growth
Homeostasis
Laboratory animals
Medical research
Microscopy
Muscle atrophy
Musculoskeletal system
Nitric oxide
Original
Oxidative stress
Penicillin
Proteins
Reactive oxygen species
Sarcopenia
Senescence
TRIM16
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Summary:Background Age‐related sarcopenia, characterized by reduced skeletal muscle mass and function, significantly affects the health of the elderly individuals. Oxidative stress plays a crucial role in the development of sarcopenia. Tripartite motif containing 16 (TRIM16) is implicated in orchestrating antioxidant responses to mitigate oxidative stress, yet its regulatory role in skeletal muscle remains unclear. This study aims to elucidate the impact of TRIM16 on enhancing antioxidant response through SIRT‐1, consequently mitigating age‐related oxidative stress, and ameliorating muscle atrophy. Methods Aged mouse models were established utilizing male mice at 18 months with D‐galactose (D‐gal, 200 mg/kg) intervention and at 24 months with natural aging, while 3‐month‐old young mice served as controls. Muscle cell senescence was induced in C2C12 myoblasts using 30 g/L D‐gal. TRIM16 was overexpressed in the skeletal muscle of aged mice and silenced/overexpressed in C2C12 myoblasts. The effects of TRIM16 on skeletal muscle mass, grip strength, morphological changes, myotube formation, myogenic differentiation, and muscle atrophy indicators were evaluated. Reactive oxygen species (ROS) levels and oxidative stress‐related parameters were measured. The SIRT‐1 inhibitor EX‐527 was employed to elucidate the protective role of TRIM16 mediated through SIRT‐1. Results Aged mice displayed significant reductions in lean mass (−11.58%; −14.47% vs. young, P 
ISSN:2190-5991
2190-6009
2190-6009
DOI:10.1002/jcsm.13553