The Pivotal Role of the Placenta in Normal and Pathological Pregnancies: A Focus on Preeclampsia, Fetal Growth Restriction, and Maternal Chronic Venous Disease

Ortega, Miguel Á.; Fraile-Martínez, Óscar; García-Montero, Cielo; Sáez, Miguel A.; Álvarez-Mon, Miguel Ángel; Torres-Carranza, Diego; Álvarez-Mon, Melchor; Buján, Julia; García‐Honduvilla, Natalio; Bravo, Coral; Guijarro, Luis G.; León-Luis, Juan De

doi:10.3390/cells11030568

Cited by 48 publications

(39 citation statements)

References 261 publications

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“…Our results indicate an aberrant expression of the transcription factor Nrf2 and its main regulators CUL-3, Keap1 and GSK-3β in the placenta tissue of women with CVD. This study gains further insights into the pathophysiological changes occurred in this organ during pregnancy, supporting the relevance of suffering from CVD as a possible obstetric complication for maternofetal wellbeing, as suggested by previous studies [ 32 , 33 ].…”

Section: Discussionsupporting

confidence: 86%

Irregular Expression of Cellular Stress Response Markers in the Placenta of Women with Chronic Venous Disease

et al. 2022

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Pregnancy comprises a period in a woman’s life in which the circulatory system is subjected to hemodynamical and biochemical changes. During this period, while restructuring blood vessels and exchanging maternal-fetal products there is an increased risk of developing chronic venous disease (CVD), which may have an echo in life after childbirth for both mother and child. Previously, we investigated that pregnancy-associated CVD involves changes in placental architecture at angiogenesis, lymphangiogenesis and villi morphology compared with healthy controls (HC) with no history of CVD. We aimed to more deeply investigate the oxidative stress response in placenta from women with CVD versus HC through several markers (NRF2, KEAP1, CUL3, GSK-3β). An observational, analytical, and prospective cohort study was conducted on 114 women in their third trimester of pregnancy (32 weeks). A total of 62 participants were clinically diagnosed with CVD. In parallel, 52 controls with no history of CVD (HC) were studied. Gene and protein expressions of NRF2, KEAP1, CUL3, GSK-3β were analyzed by real-time polymerase chain reaction (RT-qPCR) and immunohistochemistry. Nrf2 gene and protein expression was significantly greater in placental villi of women with CVD, while Keap1, CUL-3 and GSK-3β gene and protein expressions were significantly lower. Our results defined an aberrant gene and protein expression of Nrf2 and some of their main regulators Keap1, CUL-3 and GSK-3 β in the placenta of women with CVD, which could be an indicator of an oxidative environment observed in this tissue.

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Section: Discussionsupporting

confidence: 86%

Irregular Expression of Cellular Stress Response Markers in the Placenta of Women with Chronic Venous Disease

et al. 2022

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“…This leads to a persistent hypoxia/ischemia state in the placental tissue and to an imbalance in the angiogenic process which eventually leads to abnormal trophoblast behavior, oxidative stress, vascular inflammation and endocrine alterations. Eventually, systemic endothelial injury may lead to multiorgan failure and systemic complications ( Ortega et al, 2022b ). LO-PE is more likely bound to maternal extrinsic factors and, although placental damage also exists, the pathophysiological signatures, the impact of PE for both the fetus and mother, clinical features and serum markers are significantly different ( Raymond and Peterson, 2011 ).…”

Section: Placental-derived Extracellular Vesicles In Obstetric Compli...mentioning

confidence: 99%

Unfolding the role of placental-derived Extracellular Vesicles in Pregnancy: From homeostasis to pathophysiology

Ortega

Fraile-Martínez

García-Montero

et al. 2022

Front. Cell Dev. Biol.

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The human placenta is a critical structure with multiple roles in pregnancy, including fetal nutrition and support, immunological, mechanical and chemical barrier as well as an endocrine activity. Besides, a growing body of evidence highlight the relevance of this organ on the maternofetal wellbeing not only during gestation, but also from birth onwards. Extracellular vesicles (EVs) are complex macromolecular structures of different size and content, acting as carriers of a diverse set of molecules and information from donor to recipient cells. Since its early development, the production and function of placental-derived EVs are essential to ensure an adequate progress of pregnancy. In turn, the fetus receives and produce their own EVs, highlighting the importance of these components in the maternofetal communication. Moreover, several studies have shown the clinical relevance of EVs in different obstetric pathologies such as preeclampsia, infectious diseases or gestational diabetes, among others, suggesting that they could be used as pathophysiological biomarkers of these diseases. Overall, the aim of this article is to present an updated review of the published basic and translational knowledge focusing on the role of placental-derived EVs in normal and pathological pregnancies. We suggest as well future lines of research to take in this novel and promising field.

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“…Indeed, free radical species inevitably rise with cascade effects on inflammation, angiogenesis, and vascular contractility. The overexpression of free radicals and acute phase proteins is an established process in pregnancies complicated by preeclampsia or FGR, involving even severe cardiovascular effects (172,173).…”

Section: Perfusion Mismatch and Oxidative Distress Molecular Basismentioning

confidence: 99%

Endothelial dysfunction in preterm infants: The hidden legacy of uteroplacental pathologies

et al. 2022

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Millions of infants are born prematurely every year worldwide. Prematurity, particularly at lower gestational ages, is associated with high mortality and morbidity and is a significant global health burden. Pregnancy complications and preterm birth syndrome strongly impact neonatal clinical phenotypes and outcomes. The vascular endothelium is a pivotal regulator of fetal growth and development. In recent years, the key role of uteroplacental pathologies impairing endothelial homeostasis is emerging. Conditions leading to very and extremely preterm birth can be classified into two main pathophysiological patterns or endotypes: infection/inflammation and dysfunctional placentation. The first is frequently related to chorioamnionitis, whereas the second is commonly associated with hypertensive disorders of pregnancy and fetal growth restriction. The nature, timing, and extent of prenatal noxa may alter fetal and neonatal endothelial phenotype and functions. Changes in the luminal surface, oxidative stress, growth factors imbalance, and dysregulation of permeability and vascular tone are the leading causes of endothelial dysfunction in preterm infants. However, the available evidence regarding endothelial physiology and damage is limited in neonates compared to adults. Herein, we discuss the current knowledge on endothelial dysfunction in the infectious/inflammatory and dysfunctional placentation endotypes of prematurity, summarizing their molecular features, available biomarkers, and clinical impact. Furthermore, knowledge gaps, shadows, and future research perspectives are highlighted.

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The Pivotal Role of the Placenta in Normal and Pathological Pregnancies: A Focus on Preeclampsia, Fetal Growth Restriction, and Maternal Chronic Venous Disease

Cited by 48 publications

References 261 publications

Irregular Expression of Cellular Stress Response Markers in the Placenta of Women with Chronic Venous Disease

Irregular Expression of Cellular Stress Response Markers in the Placenta of Women with Chronic Venous Disease

Unfolding the role of placental-derived Extracellular Vesicles in Pregnancy: From homeostasis to pathophysiology

Endothelial dysfunction in preterm infants: The hidden legacy of uteroplacental pathologies

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