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

TY - JOUR

T1 - Keap1–Nrf2 regulated redox signaling in utero: Priming of disease susceptibility in offspring

AU - Chapple, Sarah Jane

AU - Puszyk, William M.

AU - Mann, Giovanni Enrico

PY - 2015

Y1 - 2015

N2 - Intrauterine exposure to gestational diabetes, pre-eclampsia or intrauterine growth restriction alters the redox status of the developing fetus. Such pregnancy-related diseases in most cases do not have a readily identifiablegenetic cause, and epigenetic 'priming' mechanisms in utero may predispose both mother and child to later life onset of cardiovascular and metabolic diseases. The concept of ‘fetal programing’ or ‘developmental priming’and its association with an increased risk of disease in childhood or adulthood has been reviewed extensively. This review focuses on adaptive changes in the in utero redox environment during normal pregnancy and theconsequences of alterations in redox control associated with pregnancies characterized by oxidativ estress. We evaluate the evidence that the Keap1–Nrf2 pathway is important for protecting the fetus against adverseconditions in utero and may itself be subject to epigenetic priming, potentially contributing to an increased risk of vascular disease and insulin resistance in later life.

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

M3 - Article

SN - 0891-5849

VL - 88

SP - 212

JO - Free Radical Biology and Medicine

JF - Free Radical Biology and Medicine

ER -