UCLA

Duchenne muscular dystrophy (DMD) is characterized by progressive muscle degeneration due to the absence of the protein dystrophin, and the subsequent loss of the dystrophin-glycoprotein complex, resulting in inflammation, degeneration/regeneration, and a decrease in muscular strength and function. Although the extracellular matrix was previously thought only to provide structural support to resident cells, there is a growing body of evidence implicating it in cell signaling pathways that may negatively affect muscle regeneration. Despite the increasingly acknowledged importance of the matrix, there is still very little we know about how matrix composition may change in DMD. Therefore, we utilize mass spectrometry to quantify biochemical changes that occur in the extracellular matrix in a murine model of DMD. Identification of changes in the matrisome between dystrophic and normal muscle will allow for the identification of future therapeutic targets that may inform the development of successful therapies for DMD.