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Life
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Molecular Mechanisms of Preeclampsia
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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: closed (31 December 2025) | Viewed by 7027

Special Issue Editor

Dr. Feng Li

E-Mail Website
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

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Life is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

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

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Published Papers (3 papers)

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13 pages, 3647 KB  
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
Cited by 3 | Viewed by 1963 | Correction
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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23 pages, 2844 KB  
Systematic Review
Pre-Eclampsia-Induced Maternal Liver Dysfunction: Systematic Review, Meta-Analysis and Meta-Regression of Observation Studies
by Kay-Lee E. Strauss, Wendy N. Phoswa and Kabelo Mokgalaboni
Life 2026, 16(2), 223; https://doi.org/10.3390/life16020223 - 29 Jan 2026
Viewed by 735
Abstract
Introduction: Pre-eclampsia (PE) is a pregnancy-related hypertensive condition defined by the onset of hypertension after 20 weeks of gestation that is associated with proteinuria and maternal organ damage or uteroplacental dysfunction. It continues to be a leading cause of maternal and perinatal [...] Read more.
Introduction: Pre-eclampsia (PE) is a pregnancy-related hypertensive condition defined by the onset of hypertension after 20 weeks of gestation that is associated with proteinuria and maternal organ damage or uteroplacental dysfunction. It continues to be a leading cause of maternal and perinatal morbidity and mortality globally. PE is linked to systemic inflammation, endothelial dysfunction, and oxidative stress, which may compromise hepatic function. Aim: This meta-analysis assesses the impact of PE on maternal liver function by evaluating hepatic biomarkers, including aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and total serum bilirubin. Methods: This meta-analysis of observational studies in Epidemiology (MOOSE) involved a search of PubMed and Scopus and manual screening of studies published between 2000 and 2025. Eligible studies included cross-sectional, case–control, and cohort designs. The quality of the studies was evaluated using the Newcastle–Ottawa Scale. Statistical analysis was conducted using the online meta-analysis, Jamovi version 2.6.44, and IBM SPSS Statistics version 30, and effect estimates were reported as standardized mean differences (SMDs) with 95% confidence intervals (CIs). Results: Forty-five studies, comprising 257,929 women 9420 with PE; 248,509 normotensive, were included. Women with PE had elevated AST, MD = 1.81 (95% CI: 1.51 to 2.10; p < 0.0001) and ALT, SMD = 1.73 (95% CI: 1.38 to 2.07; p < 0.0001); ALP, SMD = 1.43 (95% CI: 0.97 to 1.88; p < 0.0001); and total serum bilirubin (TSB), SMD = 0.62 (95% CI: 0.36 to 0.88; p < 0.0001) in comparison to normotensive controls. In the meta-regression, maternal age and quality were significant moderators, with older age and high-quality studies associated with smaller and larger effect sizes, respectively, for ALP (β = −0.720 and β = 1.444) and TSB (β = −0.304 and β = 0.761). For every 1-unit increase in body mass index, there was a significant 0.406-unit decrease in ALT effect size. Conclusions: PE is significantly associated with elevated maternal hepatic enzyme levels, indicating hepatocellular damage and impaired liver function. These findings emphasise the necessity for routine liver function monitoring in pregnant women with hypertensive disorders. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Preeclampsia)
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26 pages, 2631 KB  
Systematic Review
Proteome-Based Maternal Plasma and Serum Biomarkers for Preeclampsia: A Systematic Review and Meta-Analysis
by Natalia Starodubtseva, Alina Poluektova, Alisa Tokareva, Evgenii Kukaev, Anna Avdeeva, Elena Rimskaya and Zulfiya Khodzayeva
Life 2025, 15(5), 776; https://doi.org/10.3390/life15050776 - 13 May 2025
Cited by 5 | Viewed by 3528
Abstract
Proteomics has emerged as a transformative tool in biomedical research, enabling comprehensive characterization of protein profiles in complex biological systems. In preeclampsia (PE) research, quantitative proteomic analyses of plasma and serum have revealed critical insights into disease mechanisms and potential biomarkers. Through a [...] Read more.
Proteomics has emerged as a transformative tool in biomedical research, enabling comprehensive characterization of protein profiles in complex biological systems. In preeclampsia (PE) research, quantitative proteomic analyses of plasma and serum have revealed critical insights into disease mechanisms and potential biomarkers. Through a systematic review of 17 studies (2009–2024), we identified 561 differentially expressed plasma/serum proteins (p < 0.05) in PE patients versus healthy controls, with 122 proteins consistently replicated across ≥2 independent studies. Stratified analysis by clinical subtype (early-vs. late-onset PE) demonstrated both concordant and divergent protein expression patterns, reflecting heterogeneity in PE pathophysiology, methodological variations (e.g., sample processing, proteomic platforms), and differences between discovery-phase and targeted validation studies. The trimester-specific biomarker panels proposed here offer a framework for future large-scale, multicenter validation. By integrating advanced proteomic technologies with standardized preanalytical and analytical protocols, these findings advance opportunities for early prediction (first-trimester biomarker signatures); mechanistic insight (complement system involvement); and personalized management (subtype-specific therapeutic targets). This work underscores the potential of proteomics to reshape PE research, from molecular discovery to clinical translation, ultimately improving outcomes for this leading cause of maternal and perinatal morbidity. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Preeclampsia)
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