In Drosophila, intestinal stem cells (ISCs) reply to oxidative challenges and inflammation by rising proliferation The Life. . . Mortality In Addition To Estrogen Receptor inhibitor costs. This phenotype is part of a regenerative response, but can lead to hyperproliferation and epithelial degeneration within the aging animal. Here we demonstrate that Nrf2, a master regulator of the cellular redox state, particularly controls theTime. . . Death And Progestogen proliferative activity of ISCs, advertising intestinal homeostasis. We obtain that Nrf2 is constitutively lively in ISCs and that repression of Nrf2 by its unfavorable regulator Keap1 is required for ISC proliferation. We even further display that Nrf2 and Keap1 exert this function in ISCs by regulating the intracellular redox stability. Accordingly, loss of Nrf2 in ISCs causes accumulation of reactive oxygen species and accelerates age-related degeneration from the intestinal epithelium. Our findings establish Keap1 Lifestyle. . Mortality As Well As Estrogen Receptor inhibitor and Nrf2 as a crucial redox management process that regulates stem cell perform in high-turnover tissues.