Population
DBA/2J-congenic Dmdmdx mice and C57BL/10ScSn-Dmdmdx mice, along with their respective control strains
Comparison
DBA/2J genetic background (D2-mdx) vs C57BL/10ScSn genetic background (B10-mdx)
Design
Preclinical
Follow-up
between 6 and 52 weeks of age
Authors
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Identifies DBA/2J modifiers worsening γ-sarcoglycan dystrophy in mice; leaves open human translation.
The D2-mdx mouse model presents a more severe and earlier-onset dystrophic phenotype, including cardiac dysfunction, aligning with human DMD patients with the LTBP4 genetic modifier.
Coley et al. (2015) studied this question.
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