Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10737855 | Free Radical Biology and Medicine | 2015 | 24 Pages |
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 oxidative stress. 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.
Keywords
GCLNADPH:quinone oxidoreductase 1IUGRFetal programingNQO1GDMSOD1SFNNADPHRNSNrf2ROSEpigeneticscardiovascular diseaseGestational diabetes mellitusGestational diabetesType 2 diabetesSulforaphaneRedox signalingnuclear factor E2-related factor 2intrauterine growth retardationintrauterine growth restrictionnicotinamide adenine dinucleotide phosphatecornified envelopepre-eclampsiareactive nitrogen speciesReactive oxygen species
Related Topics
Life Sciences
Biochemistry, Genetics and Molecular Biology
Ageing
Authors
Sarah J. Chapple, William M. Puszyk, Giovanni E. Mann,