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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.

Type

Journal article

Journal

Neuromuscul Disord

Publication Date

04/2001

Volume

11

Pages

251 - 259

Keywords

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