1:00pm, Monday, 5 September
Room BIG13, Ground Floor
Biochemistry Building
710 Cumberland St
Dr Tanya Cully
Department of Physiology
‘Nox4 ROS, a novel therapeutic target in Duchenne Muscular Dystrophy’
Skeletal muscle function can be affected by Ca2+ regulation within a cellular microdomain known as the triad. Reactive oxygen species (ROS) also can impact muscle function via oxidative stress and the regulation of signalling cascades. The interplay between ROS and Ca2+ signalling at the triad is poorly understood and may impact the performance of healthy and diseased muscle. A mouse model of muscular dystrophy, the mdx mouse, displays both pathological increased Ca2+ leak via the Ryanodine receptor (RyR1), a calcium release channel, and increased NAD(P)H Oxidase (Nox) derived ROS.
Previously, we found that inhibiting the canonical Nox2 isoform did not decrease RyR1 Ca2+ leak in dystrophic skeletal muscle. However, inhibiting another NAD(P)H isoform, Nox4, reduced RyR1 Ca2+ leak and may be a potential therapeutic target.
