Characterizing Protein Synthesis in Dystrophic Cardiomyopathy
Duchenne muscle dystrophy (DMD) is a genetic disease that leads to fibrosis and necrosis in human striated muscles. Here, we utilized the mdx06 (dystrophic), DBko (dystrobrevin-knockout), and C06 (wild-type) mice models. Previous studies have indicated that DBko and mdx06 mice experience similar injury levels 30 hours post isoproterenol injection. In contrast, C06 mice demonstrate minimal cardiac damage, and there appears to be a median decrease in lesional percent injury 1-week post-injection as the lesional areas become fibrotic across all genotypes. Through our pilot study, we discovered a positive correlation between cardiac injury and highly concentrated protein synthesis across all genotypes. Interestingly, we observed that most high-level protein synthesis occurred remotely from lesion sites, and both immune cells and cardiac myocytes played critical roles in responding to cardiac injury. Our initial findings can provide valuable insights into how injured hearts respond to damage, allowing us to identify pathways to improve myocyte survival in DMD patients.