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Life sciences · Journal article
Clinical & Experimental Pathology · October 15, 2026
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Placental dysfunction is one of the key factors contributing to impaired intrauterine development and is considered an important mechanism of fetal programming of metabolic diseases. Its influence on the formation of fetal brown adipose tissue is of particular importance, as this tissue ensures thermogenic adaptation of the newborn and participates in the regulation of energy homeostasis. The aim of this study was to summarize current data on the impact of placental dysfunction on fetal brown adipose tissue development and to analyze the morphological, molecular, and epigenetic mechanisms underlying this process. Materials and Methods. An analysis of scientific publications indexed in the international PubMed database for the period from 2020 to 2026 was performed. The literature search was conducted using the following keywords: “placental dysfunction”, “brown adipose tissue”, “brown adipogenesis”, “fetal programming”, “maternal obesity”, “FGF21”, “PRDM16”, “UCP1”, and “epigenetics”. Among more than 180 initially identified publications, 51 sources that most fully corresponded to the topic of the study were included in this review. Results. Brown adipose tissue is a highly specialized metabolically active tissue, the development of which occurs predominantly during the antenatal period and depends on the functional state of the placenta. Placental dysfunction, through mechanisms of chronic hypoxia, oxidative stress, impaired angiogenesis, inflammatory responses, and altered nutrient transport, may affect the proliferation and differentiation of brown adipocytes. It has been shown that disruption of the UCP1, PRDM16, PPARγ, PGC-1α, and FGF21 signaling pathways plays an important role in altering the thermogenic capacity of brown adipose tissue. Changes in the expression of these molecular regulators are associated with impaired mitochondriogenesis and energy metabolism and may contribute to the development of an unfavorable metabolic phenotype in offspring. Promising approaches for assessing the impact of placental dysfunction include the application of morphological, immunohistochemical, and molecular methods with the evaluation of UCP1, PRDM16, PGC-1α, VEGF, HIF-1α, Ki-67 expression, as well as other metabolic markers. Conclusions. Placental dysfunction is an important factor capable of disrupting the morphogenesis and functional activity of fetal brown adipose tissue. The main mechanisms of this influence include hypoxia, oxidative stress, inflammation, adipokine imbalance, and alterations in key molecular pathways regulating brown adipogenesis. Comprehensive investigation of brown adipose tissue may deepen the understanding of fetal programming mechanisms and contribute to the development of new approaches for the prevention of metabolic disorders.