Custom Models of Muscle Aging

Skeletal muscle, crucial for locomotion, metabolism, and overall health, undergoes substantial age-related decline, leading to sarcopenia and impaired physical function. Age-related skeletal muscle atrophy, or sarcopenia, is a complex process involving reduced muscle mass, strength, and function. This decline stems from a multifaceted interplay of factors, including reduced protein synthesis, increased protein degradation, impaired regenerative capacity, and alterations in the muscle stem cell (also called satellite cell) niche.

Fig. 1 Comparison between rodents and zebrafish for skeletal muscle senescence. (Ichii S, et al., 2022)

CD BioSciences provides custom models of muscle aging, empowering our clients to investigate the underlying mechanisms of muscle aging, screen potential therapeutics, and accelerate the development of innovative interventions.

Why Use Skeletal Muscle as an Experimental Model to Study Tissue Aging?

• Accessibility. Skeletal muscle is readily accessible for biopsy and experimentation.
• Regenerative capacity. Skeletal muscle possesses a remarkable regenerative capacity, allowing the study of age-related changes.

Our Aging Skeletal Muscle Modeling Services

CD BioSciences employs various techniques to develop custom aging skeletal muscle models, catering to diverse research needs. Our expertise encompasses a range of in vitro and in vivo models.

In vitro models of aging skeletal muscle

CD BioSciences offers custom aging skeletal muscle cell models using both primary myocytes and immortalized cell lines. Our models replicate the key characteristics of senescent muscle cells, allowing clients to assess the effects of aging on myotube formation, protein synthesis, and protein degradation. Using these in vitro models, our clients can investigate cellular responses to aging, explore the therapeutic effects of anti-aging interventions, and assess the efficacy of interventions to alleviate muscle degeneration.

Rodent models for skeletal muscle senescence

At CD BioSciences, we offer rodent models to support clients in studying age-related changes in muscle mass, strength, function, and fiber type composition.

• Our company provides custom models using naturally aged rodents or inducing accelerated aging using caloric restriction mimetics, D-galactose (D-gal), and dexamethasone (DEX).
• We offer genetically engineered mice, such as LmnaL^530P/L530P, Bub1b^H/H, Bub1b^+/GTTA, p53^+/m, Bmal1^−/−, and Rps9 D95N, which depict loss of muscle, reduction of muscle fiber widths, and degeneration of skeletal muscle.
• We provide hindlimb unloading models, mimicking the effects of disuse atrophy, a significant contributor to sarcopenia. Our experts tailor the unloading period and protocols to meet the specific research objectives.
• We also offer services to customize mouse models for peripheral denervation, involving implementation of surgical denervation, control of denervation duration, and assessment of muscle atrophy parameters.

Zebrafish models for skeletal muscle senescence

Zebrafish, with their optical transparency and genetic tractability, offer unique advantages for studying skeletal muscle aging. CD BioSciences develops custom zebrafish models that allow for high-throughput screening of potential therapeutics and real-time visualization of age-related changes in muscle structure and function. Our experts support clients in establishing zebrafish aging models by subjecting them to chronic alcohol exposure, which reliably induces significant skeletal muscle atrophy. We also offer comprehensive services to characterize zebrafish aging models and perform detailed analyses of muscle morphology.

CD BioSciences empowers clients to explore the mechanism of muscle aging and develop effective therapeutics by providing custom cell, rodent, and zebrafish models. If you are interested in our services, please feel free to contact us or make an online inquiry.

Reference

1. Ichii S, et al. Zebrafish Models for Skeletal Muscle Senescence: Lessons from Cell Cultures and Rodent Models. Molecules, 2022, 27 (23): 8625.