The role of reactive oxygen species in the hearts of dystrophin-deficient mdx mice

PubMed, the Internet portal of biomedical and life sciences literature, indexed an interesting article, entitled The role of reactive oxygen species in the hearts of dystrophin-deficient mdx mice. ( Am J Physiol Heart Circ Physiol. 2007 Sep;293(3):H1969-77.). Authors are Williams IA and Allen DG from the Bosch Institute, School of Medical Sciences, University of Sydney F13, NSW 2006 Australia. Duchenne muscular dystrophy (DMD) is caused by deficiency of the cytoskeletal protein dystrophin. Oxidative stress is thought to contribute to the skeletal muscle damage in DMD; however, little is known about the role of oxidative damage in the pathogenesis of the heart failure that occurs in DMD patients. The dystrophin-deficient (mdx) mouse is an animal model of DMD that also lacks dystrophin. The current study investigates the role of the antioxidant N-acetylcysteine (NAC) on mdx cardiomyocyte function, Ca(2+) handling, and the cardiac inflammatory response.Therapies designed to reduce oxidative damage might be beneficial to DMD patients with heart failurе. To access the full abstract of the article, click here.