Pathomechanisms of Prenatally Programmed Adult Diseases

Antioxidants (Basel). 2023 Jun 28;12(7):1354. doi: 10.3390/antiox12071354.

Abstract

Based on epidemiological observations Barker et al. put forward the hypothesis/concept that an adverse intrauterine environment (involving an insufficient nutrient supply, chronic hypoxia, stress, and toxic substances) is an important risk factor for the development of chronic diseases later in life. The fetus responds to the unfavorable environment with adaptive reactions, which ensure survival in the short run, but at the expense of initiating pathological processes leading to adult diseases. In this review, the major mechanisms (including telomere dysfunction, epigenetic modifications, and cardiovascular-renal-endocrine-metabolic reactions) will be outlined, with a particular emphasis on the role of oxidative stress in the fetal origin of adult diseases.

Keywords: epigenetic modifications; metabolic hormones; nutrition; oxidative stress; perinatal programming; placental function.

Publication types

  • Review

Grants and funding

This research was funded by the European Union (EU) RRF-2.3.1-21-2022-00012 “National Laboratory on Human Reproduction” project, at the University of Pecs, Hungary.