Enhanced dimethylarginine degradation improves coronary flow reserve and exercise tolerance in Duchenne muscular dystrophy carrier mice

Duchenne muscular dystrophy (DMD) carriers are at risk for cardiomyopathy. The nitric oxide synthase inhibitor asymmetric dimethylarginine (ADMA) is released from damaged muscle in DMD and impairs exercise performance. Transgenic expression of dimethylarginine dimethylaminohydrolase to degrade ADMA...

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Veröffentlicht in:	American journal of physiology. Heart and circulatory physiology 2020-09, Vol.319 (3), p.H582-H603
Hauptverfasser:	Garbincius, Joanne F., Merz, Lauren E., Cuttitta, Ashley J., Bayne, Kaitlynn V., Schrade, Sara, Armstead, Emily A., Converso-Baran, Kimber L., Whitesall, Steven E., D’Alecy, Louis G., Michele, Daniel E.
Format:	Artikel
Sprache:	eng
Schlagworte:	Arginine Asymmetry Blood circulation Blood flow Cardiac function Cardiomyopathy Damage Degeneration Degradation Dimethylargininase Duchenne's muscular dystrophy Dystrophin Dystrophy Fatigue Heart Hypertrophy Metabolism Muscles Muscular dystrophy Muscular fatigue Mutation Nitric oxide Nitric-oxide synthase Skeletal muscle Transgenic mice Weight reduction
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