Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

Dilated cardiomyopathy is a common complication of Duchenne and Becker muscular dystrophies, which are caused by mutations in the dystrophin gene. The mdx mouse is an animal model for Duchenne muscular dystrophy (DMD) and shows mildly dystrophic changes in the heart. By contrast, the utrophin-dystrophin knockout (dko) mouse shows severe dystrophic changes in cardiac muscle, that more closely resembles DMD cardiomyopathy than mdx mouse. However the pathogenesis of development has not been fully understood. Recently many reports have revealed that calcineurin and stress activated protein kinase (SAPK)/p38-mitogen activated protein kinase (MAPK) hypertrophic signalling pathways are associated with the development of some forms of hypertrophic and dilated cardiomyopathies. These signalling pathways may have some roles in the development of dystrophin-deficient cardiomyopathy. Here we report that calcineurin and SAPK/p38-MAPK signalling pathways were constantly activated in dko hearts, but the activation varied in mdx hearts. The pathogenesis of the development of dystrophin-deficient cardiomyopathy may be associated with the activation of these signalling pathways.


Journal article


Neuromuscul Disord

Publication Date





251 - 259


Age Factors, Animals, Atrial Natriuretic Factor, Calcineurin, Cardiomyopathy, Dilated, Cytoskeletal Proteins, Dystrophin, Glyceraldehyde-3-Phosphate Dehydrogenases, Membrane Proteins, Mice, Mice, Inbred C57BL, Mice, Knockout, Mitogen-Activated Protein Kinase 8, Mitogen-Activated Protein Kinases, Muscular Dystrophy, Duchenne, Myocardium, Natriuretic Peptide, Brain, RNA, Messenger, Receptor, Angiotensin, Type 1, Receptor, Angiotensin, Type 2, Receptors, Angiotensin, Signal Transduction, Utrophin, p38 Mitogen-Activated Protein Kinases