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

Research output: Contribution to journalArticlepeer-review

26 Citations (Scopus)

Abstract

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 identifiable
genetic 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 the
consequences 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 adverse
conditions 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.
Original languageEnglish
Pages (from-to)212
Number of pages220
JournalFree Radical Biology and Medicine
Volume88
Publication statusPublished - 2015

Fingerprint

Dive into the research topics of 'Keap1–Nrf2 regulated redox signaling in utero: Priming of disease susceptibility in offspring'. Together they form a unique fingerprint.

Cite this