Pathomechanisms of Prenatally Programmed Adult Diseases

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.

Automated summary

Based on epidemiological observations, Barker et al. proposed the hypothesis/concept that adverse intrauterine environment, including insufficient nutrient supply, chronic hypoxia, stress, and toxic substances, is a significant risk factor for the development of chronic diseases in adulthood. Fetus responds to the unfavorable environment with adaptive reactions, ensuring short-term survival, but initiating pathological processes leading to adult diseases. This review outlines major mechanisms, such as telomere dysfunction, epigenetic modifications, and cardiovascular-renal-endocrine-metabolic reactions, with a particular focus on the role of oxidative stress in fetal origin of adult diseases.