Impact of oxidative stress during pregnancy on fetal epigenetic patterns and early origin of vascular diseases.

Abstract

Epidemiological studies have led scientists to postulate the developmental origins of health and disease hypothesis for noncommunicable diseases such as diabetes, cardiovascular diseases, hypertension, and obesity. However, the cellular and molecular mechanisms involved in the development of these diseases are not well understood. In various animal models, it has been observed that oxidative stress during pregnancy is associated with the early development of endothelial dysfunction in offspring. This phenomenon suggests that endothelial dysfunction may initiate in the uterus and could lead to increased risk of cardiovascular disease later in life. Currently, it is known that many of the fetal adaptive responses to environmental factors are mediated by epigenetic changes in the genome, especially by the degree of methylation in cytosines in the promoter regions of genes. These findings suggest that the establishment of a particular epigenetic pattern in the genome may be generated by oxidative stress.