Ryanodine receptor dysfunction causes senescence and fibrosis in Duchenne dilated cardiomyopathy

• Ngā kaituhi matua: Monia Souidi (Author), Jessica Resta (Author), Haikel Dridi (Author), Yvonne Sleiman (Author), Steve Reiken (Author), Karina Formoso (Author), Sarah Colombani (Author), Pascal Amédro (Author), Pierre Meyer (Author), Azzouz Charrabi (Author), Marie Vincenti (Author), Yang Liu (Author), Rajesh Kumar Soni (Author), Frank Lezoualc'h (Author), D.V.M. Stéphane Blot (Author), François Rivier (Author), Olivier Cazorla (Author), Angelo Parini (Author), Andrew R. Marks (Author), Jeanne Mialet‐Perez (Author), Alain Lacampagne (Author), Albano C. Meli (Author)
• Hōputu: Pukapuka
• I whakaputaina: Wiley, 2024-04-01T00:00:00Z.
• Ngā marau: article
• Urunga tuihono: Connect to this object online.

Abstract Background Duchenne muscular dystrophy (DMD) is an X‐linked disorder characterized by progressive muscle weakness due to the absence of functional dystrophin. DMD patients also develop dilated cardiomyopathy (DCM). We have previously shown that DMD (mdx) mice and a canine DMD model (GRMD) e...