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Myocardial infarction (MI)-induced heart failure is characterized by central nervous system-driven sympathoexcitation and deteriorating cardiac function. The paraventricular nucleus (PVN) of the hypothalamus is a key regulator of sympathetic nerve activity and is implicated in heart failure. Redox signaling in the PVN and other central nervous system sites is a primary mechanism of neuro-cardiovascular regulation, and excessive oxidant production by activation of NADPH oxidases (Noxs) is implicated in some neuro-cardiovascular diseases.

circulation research

Silencing Nox4 in the Paraventricular Nucleus Improves Myocardial Infarction–Induced Cardiac Dysfunction by Attenuating Sympathoexcitation and Periinfarct Apoptosis