Molecular Mechanisms of Preeclampsia

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Reproductive and Developmental Biology".

Deadline for manuscript submissions: 30 April 2025 | Viewed by 785

Special Issue Editor


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Guest Editor
Department of Pathology and Laboratory Medicine, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7525, USA
Interests: roles of maternal genetic factors in preeclampsia and trophoblast biology; the beneficial effects of small molecules (e.g., nicotinamide) on preeclampsia and associated mechanisms

Special Issue Information

Dear Colleagues,

Preeclampsia is a pregnancy-related disorder, characterized by maternal hypertension, proteinuria and end-organ damage. It affects approximately 5–8% of all pregnancies and is a leading cause of both maternal and neonatal morbidity and mortality. The mothers and children of preeclamptic pregnancies are at increased risk for cardiovascular diseases and cognitive disorders later in life. Currently, there is no effective way to predict and treat preeclampsia; the ultimate treatment is delivery of the baby and placenta as physicians did a century ago.

Various molecules and pathways are involved in preeclampsia pathogenesis. The aim of this Special Issue is to provide an overview of the molecules and pathways involved in preeclampsia in order to better understand the molecular mechanisms of this disorder and identify potential targets for intervention. We are welcoming submissions of original research articles and reviews on topics relevant to any aspect of preeclampsia pathogenesis.

Dr. Feng Li
Guest Editor

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Keywords

  • preeclampsia
  • hypertension
  • proteinuria
  • placenta
  • fetal growth restriction
  • pregnancy com-plications
  • implantation

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Published Papers (1 paper)

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Research

13 pages, 3646 KiB  
Article
Inhibitor of DNA Binding Protein 2 (ID2) Mediates the Anti-Proliferative and Pro-Differentiation Effects of Insulin-like Growth Factor-1 (IGF-1)
by Rebecca Ssengonzi, Yuye Wang, Jiayi Zhou, Yukako Kayashima, W. H. Davin Townley-Tilson, Balaji Rao, Qing Ma, Nobuyo Maeda-Smithies and Feng Li
Life 2024, 14(12), 1663; https://doi.org/10.3390/life14121663 - 16 Dec 2024
Viewed by 406
Abstract
In preeclampsia (PE), impaired trophoblast proliferation and differentiation are thought to cause abnormal placentation and subsequent clinical manifestations of the disease, i.e., hypertension, proteinuria, and end-organ damage. Insulin-like growth factor-1 (IGF-1) influences trophoblast cell function; however, the mechanism of IGF-1’s action on trophoblasts [...] Read more.
In preeclampsia (PE), impaired trophoblast proliferation and differentiation are thought to cause abnormal placentation and subsequent clinical manifestations of the disease, i.e., hypertension, proteinuria, and end-organ damage. Insulin-like growth factor-1 (IGF-1) influences trophoblast cell function; however, the mechanism of IGF-1’s action on trophoblasts is not understood well. Inhibitor of DNA binding protein 2 (ID2) is involved in trophoblast differentiation and implicated in many processes disrupted in PE, including placental development, vascular differentiation, and angiogenesis. We hypothesized that IGF-1 regulates trophoblast proliferation and differentiation via ID2. Immortalized human first trimester trophoblast cells (HTR-8/SVneo) were treated with IGF-1 for 24 h after serum starvation. ID2 mRNA and protein were measured, as well as trophoblast cell viability, proliferation, tube formation, and migration. IGF-1 decreased ID2 expression in a dose-dependent manner. IGF-1 decreased trophoblast proliferation but increased cell viability, differentiation, and migration. ID2 overexpression mitigated the effects of IGF-1 on trophoblast cells. These data suggest that IGF-1 could regulate trophoblast proliferation and differentiation through ID2. The dysregulation of ID2-mediated IGF-1 signaling in trophoblast cells could be involved in the pathogenesis of pregnancy disorders like uterine growth restriction and PE. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Preeclampsia)
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