Constitutive activation of Nrf2 induces a stable reductive state in the mouse myocardium.

ABSTRACT: Redox homeostasis regulates key cellular signaling pathways in both physiology and pathology. The cell's antioxidant response provides a defense against oxidative stress and establishes a redox tone permissive for cell signaling. The molecular regulation of the well-known Keap1/Nrf2 system acts as sensor responding to changes in redox homeostasis and is poorly studied in the heart. Importantly, it is not yet known whether Nrf2 alone can serve as a master regulator of cellular redox homeostasis without compensation of the transcriptional regulation of antioxidant response element (ARE) genes through alternate mechanisms. Here, we addressed this question using cardiac-specific transgenic expression at two different levels of constitutively active nuclear erythroid related factor 2 (caNrf2) f

SUBMITTER: Shanmugam G 

PROVIDER: S-EPMC5423345 | biostudies-literature | 2017 Aug

REPOSITORIES: biostudies-literature