West JD, Galindo CL, Kim K, et al. – Researchers determined whether thromboxane-prostanoid receptor (TPr) activation contributes to the cardiac phenotype of muscular dystrophy (MD) in this investigation. They also determined if cardiac fibrosis and function could be improved by TPr antagonism in preclinical models of MD. They used mdx/utrn (utrophin) double knockout, second generation mdx/mTR double knockout, and delta-sarcoglycan knockout as three different mouse models of MD. These models were delivered normal drinking water or water containing 25 mg/kg per day of the TPr antagonist ifetroban, commenced at weaning. Following 6 months (10 weeks for mdx/utrn double knockout), they assessed the mice for cardiac and skeletal muscle function prior to euthanization. Findings revealed that cardiomyopathy and spontaneous death in mouse models of Duchenne and limb-girdle MD were reduced as a result of TPr antagonism. On the basis of these investigations, ifetroban and other TPr antagonists could serve as new therapeutics for the management of the cardiac phenotype in patients with MD.