Rachelle H. Crosbie

The paper shows that collagen abundance alone does not define fibrosis in DMD, as distinct matrix states with different biological activities and mechanosignaling exist.

This study uses multi-omics analysis to show that sarcospan overexpression in mdx mice compensates for dystrophin deficiency by altering cytoskeleton-matrix interactions and mechanotransduction pathways.

The paper shows that different forms of muscular dystrophy have distinct ECM compositions that affect myoblast motility, with annexin A6 playing a key role in enhancing movement.