Population
Heart cells (cardiomyocytes) and a mouse model of Duchenne muscular dystrophy
Design
Preclinical
Authors
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May promote stretch-induced arrhythmias in DMD models; hypothesis-generating for NOX2-targeted therapies with no clinical implications yet.
Identifies X-ROS signaling as a microtubule-dependent mechanism linking mechanical stretch to NOX2-mediated ROS production and RyR sensitization, contributing to arrhythmogenic Ca2+ release in Duchenne muscular dystrophy.
Prosser et al. (2011) studied this question.
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