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RNA-seq analysis for the Fluo-4 abnormal myofibers in aged mice

ABSTRACT: In a rapidly aging society, the age-related decline in muscle mass and force, sarcopenia, is an urgent medical and economic issue. However, the molecular mechanisms of sarcopenia are still largely unknown. Using Ca2+ indicator Fluo-4, we identified the presence of the Fluo-4 abnormal muscle fibers only in aged mice. The Fluo-4 abnormal muscle fibers had a tubular aggregate-like structure and morphologically abnormal mitochondria. Furthermore, a cluster of mitochondria-related genes, including mitochondrially-encoded genes, were downregulated in Ca2+-abnormal muscle fibers. These results indicate that the Fluo-4 abnormal muscle fibers are accumulated in aged mice, and that age-related mitochondrial abnormalities are more prominent in these fibers.

ORGANISM(S): Mus musculus

PROVIDER: GSE300563 | GEO | 2026/04/23

REPOSITORIES: GEO

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Project description:The degenerative loss of muscle associated with aging leading to muscular atrophy is called sarcopenia. Currently, practicing regular physical exercise is the only efficient way to delay the onset of sarcopenia. To identify therapeutic targets to suppress the symptoms of aging, there is a need for in vivo model organisms of accelerated muscle degeneration and atrophy. The zebrafish harbors hallmarks of aging, notably mitochondrial dysfunction, telomeres shortening and accumulation of senescent cells. Unfortunately, zebrafish aged slowly, and no specific zebrafish models of accelerated muscle atrophy associated with aging or sarcopenia are currently available. We have developed a new genetic tool to efficiently accelerate muscle fibers degeneration and muscle tissue atrophy in zebrafish larvae and adults. We used a gain-of-function strategy with a molecule that has been shown to be necessary and sufficient to induce muscle atrophy and a sarcopenia phenotype in mammals: Atrogin1 (also named Fbxo32). We report the generation, validation, and characterization of a zebrafish genetic model of accelerated muscle atrophy, the sarcofish. We demonstrated that specific expression of Atrogin1 in skeletal muscle tissue induces a muscle atrophic phenotype associated with locomotion dysfunctions in both larvae and adult fish. We identified that degradation of the myosin light chain as an event occurring before the degeneration of muscle fibers. Biological processes associated with muscle aging such as inflammation, proteolysis, apoptosis and stress response are upregulated in the sarcofish. Surprisingly, we observed a strong correlation between muscle fibers degeneration and a reduction of neuromuscular junctions in the peripheral nervous system, as well as neuronal cell bodies in the spinal cord, suggesting that muscle atrophy could underly a neurodegenerative phenotype in the central nervous system. Finally, while sarcofish larvae harbor regeneration of muscle fibers, spinal neurons and recover locomotive functions, adult sarcofish have impaired regenerative capacities as observed in mammals during muscle aging. In the future, the sarcofish could open new strategies in the fight against the sarcopenia disease to test therapeutic molecules aiming to treat or alleviate the symptoms of muscle aging.

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RNA-seq analysis for the Fluo-4 abnormal myofibers in aged mice

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