Studying intramuscular fat deposition and muscle regeneration: insights from a comparative analysis of mouse strains, injury models, and sex differences

Skeletal Muscle, 2024 · DOI: https://doi.org/10.1186/s13395-024-00344-4 · Published: May 13, 2024

Physiology Regenerative Medicine & Stem Cells Musculoskeletal Medicine

Simple Explanation

This study compares how different mouse strains, sexes, and injury types affect fat accumulation in muscle, muscle regeneration, and scar tissue formation. The researchers found that some mouse strains are more prone to fat accumulation, females tend to accumulate more fat than males after certain injuries, and the type of injury also affects fat and scar tissue formation. These findings help researchers choose the best mouse model for studying muscle diseases that involve fat accumulation.

Study Duration

Not specified

Participants

Three widely used mouse strains: C57BL/6J, 129S1/SvlmJ and CD1

Evidence Level

Not specified

Key Findings

1
Bl6 mice are more resistant to IMAT formation compared to 129S and CD1 strains.
2
Females of all strains had a higher adipogenic capacity than males after Glycerol (GLY) injury.
3
129S mice were the most resistant to injury-induced fibrosis.

Research Summary

The study investigates the impact of mouse strain, sex, and injury type on intramuscular fat (IMAT) formation, myofiber regeneration, and fibrosis. Results show that C57BL/6J mice are resistant to IMAT, while 129S1/SvlmJ and CD1 strains are more susceptible. Females form more IMAT than males after a Glycerol injury. Myofiber regeneration is strain-dependent, with C57BL/6J showing complete regeneration. IMAT and fibrosis are negatively correlated with myofiber regeneration.

Practical Implications

Model Selection

Researchers should carefully consider mouse strain, sex, and injury model when studying IMAT formation.

Translational Relevance

Understanding strain-specific differences can improve the translational relevance of preclinical studies.

Genetic Modifiers

Identifying genetic modifiers responsible for IMAT formation could uncover novel genetic predispositions to IMAT in humans.

Study Limitations

1
Mice are extremely lean and require exogenous perturbation to induce IMAT.
2
Injectable muscle injuries are an artificial stimulus and do not directly model the human condition.
3
Phenotypic similarities in IMAT do not always predict better modeling of human pathology.

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