Figure 1

The MRL genome suppresses fibrosis in the heart and muscles of Sgcg^D2mice. Sgcg mice lack the dystrophin-associated protein, γ-sarcoglycan, and when in the DBA/2J (D2) background have a more severe phenotype with enhanced membrane leak and fibrosis[21]. A 50% contribution of the MRL genome, referred to as Sgcg^MRL/D2, suppressed fibrosis in both heart and skeletal muscle.