Pressure-overload induced subcellular re-localization/oxidation of soluble guanylate cyclase in the heart modulates enzyme stimulation

摘要

RationaleSoluble guanylyl cyclase (sGC) generates cyclic guanosine monophophate (cGMP) upon activation by nitric oxide (NO). Cardiac NO-sGC-cGMP signaling blunts cardiac stress responses, including pressure-overload induced hypertrophy. The latter itself depresses signaling via this pathway by reducing NO generation and enhancing cGMP hydrolysis.