A role for the transcription factor NRF2 in the prevention of salt-induced vascular dysfunction

In the United States, the average adult consumes more than twice the amount of daily sodium recommended by the American Heart Association. Even short-term salt consumption impairs endothelial function in humans, which serves as an independent risk factor for cardiovascular morbidity and mortality, and occurs independent of an increase in blood pressure. Our work suggests that the transcription factor NRF2 may play a critical role in the protection against vascular damage by salt-mediated ANG II suppression via the maintenance vascular redox homeostasis. This presents a novel therapeutic target in the prevention and treatment of endothelial dysfunction that underlies a variety of pathologies, including cardiovascular disease. (Abstract shortened by UMI.).