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Nitric oxide activation of soluble guanylyl cyclase (sGC) blunts the cardiac stress response, including cardiomyocyte hypertrophy. In the concentric hypertrophied heart, oxidation and re-localization of myocardial sGC diminish cyclase activity, thus aggravating depressed nitric oxide–cyclic guanosine monophosphate (NO–cGMP) signaling in the pressure-overloaded failing heart. Here, we hypothesized...
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