EDMD-causing emerin mutants showed significantly decreased expression for collagen, laminin, von Willebrand factor, thrombospondin 1, reelin, and vitronectin, revealing alterations in the ECM–receptor pathway needed for regulation of cellular events vital for muscle growth, repair and to mediate cell–cell adhesion during skeletal muscle regeneration. Here, VTN is linked to Emery-Dreifuss muscular dystrophy.