Abstract
Early-life stressful experiences are critical for plasticity and development, shaping adult neuroendocrine response and future health. Stress response is mediated by the autonomous nervous system and the hypothalamic–pituitary–adrenal (HPA) axis while various environmental stimuli are encoded via epigenetic marks. The stress response system maintains homeostasis by regulating adaptation to the environmental changes. Pre-conceptual and in utero stressors form the fetal epigenetic profile together with the individual genetic profile, providing the background for individual stress response, vulnerability, or resilience. Postnatal and adult stressful experiences may act as the definitive switch. This review addresses the issue of how preconceptual in utero and postnatal events, together with individual differences, shape future stress responses. Putative markers of early-life adverse effects such as prematurity and low birth weight are emphasized, and the epigenetic, mitochondrial, and genomic architecture regulation of such events are discussed.
Highlights
Zoe Papadopoulou 1, Angeliki-Maria Vlaikou 1,2, Daniela Theodoridou 1, Georgios S
Stress response is mediated by the autonomous nervous system and the hypothalamic–pituitary–adrenal (HPA) axis while various environmental stimuli are encoded via epigenetic marks
This review addresses the issue of how preconceptual in utero and postnatal events, together with individual differences, shape future stress responses
Summary
Intrauterine life events may have a much greater impact on epigenetic profiles than stressful exposures during adult life [12]. Anxiety, and depression during pregnancy are considered in utero adverse experiences and have been associated with low birth weight (LBW) and future health problems [16,17,18,19,20,21,22,23,24]. LBW, apart from being a risk factor for neonatal morbidity and mortality, has been proposed as a marker of early-life adversities [25, 26]. In this mini-review, genetic and epigenetic factors that shape stress response are discussed. The contribution of mitochondria and individual predisposition to developing mental health problems in response to a stressful stimulus will be addressed
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