Duchenne muscular dystrophy (DMD) is a progressive, muscle-wasting disease where cell membrane instability continually damages muscle fibers due to an absence of the protein dystrophin. DMD-associated cardiomyopathy is the leading cause of death in patients with DMD and has limited treatment options. Cardiomyocyte death in the heart leads to increased fibrosis, dilation of the cardiac cavities, and decreased contractile function. I am examining the use of a porcine-derived myocardial matrix hydrogel in mdx mice, a murine model for DMD, in order to promote extracellular matrix (ECM) remodeling and improve cardiac function. This hydrogel has shown anti-fibrotic effects in the heart post myocardial infarction (MI) in pre-clinical models and a phase I clinical trial. To assess the effects of the matrix hydrogel, I measured the abundance of ECM proteins, quantified macrophage populations and optimized a surgical procedure for echocardiography-guided direct cardiac injection of the matrix hydrogel. We optimized a less invasive protocol for injections and observed a change in the endogenous ECM’s architecture.