Keap1-Nrf2 regulated redox signaling in utero: Priming of disease susceptibility in offspring.

摘要: Intrauterine exposure to gestational diabetes, pre-eclampsia or intrauterine growth restriction alters the redox status of developing fetus. Such pregnancy-related diseases in most cases do not have a readily identifiable genetic cause, and epigenetic 'priming' mechanisms utero may predispose both mother child later-life onset cardiovascular metabolic diseases. The concept 'fetal programing' 'developmental priming' its association with an increased risk disease childhood adulthood has been reviewed extensively. This review focuses on adaptive changes environment during normal pregnancy consequences alterations control associated pregnancies characterized by oxidative stress. We evaluate evidence that Keap1-Nrf2 pathway is important for protecting fetus against adverse conditions itself be subject priming, potentially contributing vascular insulin resistance later life.