La interfaz materno-placentario-fetal: Adaptaciones del Eje Hipotálamo Hipofisario Adrenal, los mediadores inmunitarios post estrés materno y la exposición prenatal al alcohol

I Rabinovich Orlandi

Vol. 33 No. 1 (2026), Critical Analysis of the Bibliography

Vol. 33 No. 1 (2026)

The maternal-placental-fetal interface: Adaptations of the hypothalamic-pituitary-adrenal (HPA) axis and immune mediators following maternal stress and prenatal alcohol exposure

Critical Analysis of the Bibliography

Published 2026-01-31

I Rabinovich Orlandi⁺⁻

I Rabinovich Orlandi

Universidad de Buenos Aires, Facultad de Medicina, Cátedra de Embriología, Ciudad Autónoma de Buenos Aires, Argentina.

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Keywords

maternal-placental-fetal interface
hypothalamic-pituitary-adrenal

How to Cite

1.

Rabinovich Orlandi I. The maternal-placental-fetal interface: Adaptations of the hypothalamic-pituitary-adrenal (HPA) axis and immune mediators following maternal stress and prenatal alcohol exposure. RSAEGRE [Internet]. 2026 Jan. 31 [cited 2026 Apr. 17];33(1):47-53. Available from: http://revistasaegre.com.ar/index.php/revista/article/view/54

Abstract

This review addresses underlying physiological, cellular, and molecular factors that alter the developing fetal brain stress circuits and responses of the hypothalamic-pituitary-adrenal (HPA) axis caused by maternal stress and prenatal alcohol exposure (PAE). An emphasis is placed on the contribution of the placenta following maternal stress separately, and as a co-occurrence with PAE. Altered fetal HPA axis ultimately results in dys regulation of the brain stress-response system long after birth and possibly lifelong. Additional consideration of the role of placentally-derived endocrine and sex hormones, as well as a brief discussion of epigenetic mecha nisms of altered placental expression of genes encoding the glucocorticoid receptor and the enzymes 11β-HSD that rapidly convert glucocorticoids into its active or inactive forms are reviewed. Data highlighting the strong, reciprocal interactions between the neuroimmune and neuroendocrine systems during fetal development that are impacted by maternal stress and PAE are considered, emphasizing the role of the placenta as a key contributor to the dysregulation of these systems. In view of the maternal-placentalfetal interface, important physiological, cellular, and molecular factors underlying later life dysregulated stress responses are additionally considered. Literature from animal models of PAE and maternal stress is reviewed that support clinical observations of the effect of maternal stress and alcohol exposure during fetal development on later-life adult stress responses and associated mood dysregulation. An appreciation of dysregulated stress responses in individuals with fetal alcohol spectrum disorders (FASD) are addressed given the greater prevalence of adult dysregulated stress responses and a greater co-occurrence of mood disorders in individuals diagnosed with FASD.

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