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Advanced Molecular Research on Hypertensive Disorders of Pregnancy (HDPs)
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Advanced Molecular Research on Hypertensive Disorders of Pregnancy (HDPs)

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 31 August 2025 | Viewed by 3930

Special Issue Editor

Dr. Melissa Wilson

E-Mail Website
Guest Editor
Department of Population and Public Health Sciences, Keck School of Medicine of USC, Los Angeles, CA, USA
Interests: preeclampsia; genetics; maternal-fetal medicine; HELLP syndrome; developmental origins of health and disease; pregnancy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Molecular epidemiology is a burgeoning area of research into causal factors associated with hypertensive disorders of pregnancy (HDP). While much research into the etiology of HDP has been conducted, the underlying causes of HDP have yet to be elucidated. Recent technological advances have allowed for a wide array of new methods by which the causes of HDP, and subsequent long-term risks, can be investigated. Understanding how HDP develops is essential to developing methods to prevent or treat the condition and to reduce long-term risks for both the mother and her child.

We are pleased to invite you to submit a manuscript for this Special Issue. Current Issues in Molecular Biology is an international, scientific, peer-reviewed, open-access journal covering topics in molecular biology and published online monthly. We cover a wide range of topics, including molecular biology, microbiology, genetics and genomics, informatics, and reproductive biology.

With this Special Issue, we aim to focus on cutting-edge molecular-based research in the field of HDP. As noted, all article types will be considered for publication, provided that they address a human population. Some themes might include, but are not limited to, genetic association studies, gene expression, epigenetics, protein levels, mitochondrial DNA, and alterations in the microbiome that may be related to the risk or early detection of HDP.

We look forward to receiving your contributions.

Dr. Melissa Wilson
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 100 words) can be sent to the Editorial Office for announcement on this website.

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. Current Issues in Molecular Biology 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 2200 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

  • DNA
  • RNA
  • protein
  • microbiome
  • hypertensive disorders of pregnancy
  • preeclampsia
  • epidemiology
  • meta-analysis

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Published Papers (4 papers)

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Research

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12 pages, 1112 KiB  
Article
Stimulation of Angiotensin II Receptor Subtype 2 Reduces Preeclampsia-like Symptoms in a Mouse Model of Preeclampsia
by Keiichi Matsubara, Yuko Matsubara, Yuka Uchikura and Takashi Sugiyama
Curr. Issues Mol. Biol. 2024, 46(9), 9760-9771; https://doi.org/10.3390/cimb46090579 - 2 Sep 2024
Viewed by 1097
Abstract
Angiotensin II (AngII) receptor subtype 1 (AT1R) is involved in the pathogenesis of preeclampsia (PE). Angiotensin II receptor subtype 2 (AT2R) can antagonize the effects of AT1R, but its effects during pregnancy are not known. We investigated the effect of AT2R on the [...] Read more.
Angiotensin II (AngII) receptor subtype 1 (AT1R) is involved in the pathogenesis of preeclampsia (PE). Angiotensin II receptor subtype 2 (AT2R) can antagonize the effects of AT1R, but its effects during pregnancy are not known. We investigated the effect of AT2R on the pathogenesis of PE using a mouse model and recently developed AT2R agonist (compound 21 [C21]). Blastocysts collected from pregnant imprinting control region (ICR) mice were incubated with adenovirus containing the CD40L gene and transferred into the uterine horns of pseudo-pregnant ICR mice to express PE-like features. Osmotic pumps were placed subcutaneously on the dorsal side with C21 or saline. C21 reduced the plasma soluble fms-like tyrosine kinase 1 (sFlt-1) concentration, ameliorating hypertension. The splenic T and B cell profiles in model mice were analyzed by flow cytometry. The gated percentage of IFN-γ-positive Th cells was significantly increased and the percentage of plasma cells in B cells was significantly decreased; however, the percentages were not altered by C21. sFlt-1 and soluble endoglin concentrations in plasma were measured with an enzyme-linked immunosorbent assay, and sFlt-1 was reduced. C21 could become a candidate PE drug as it ameliorated the pathophysiology of PE as a result of decreased production of sFlt-1. Full article
(This article belongs to the Special Issue Advanced Molecular Research on Hypertensive Disorders of Pregnancy (HDPs))
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19 pages, 4686 KiB  
Article
Association between Maternal and Fetal Genetic Variants and Preeclampsia: Evidence from a Meta-Analysis
by Tung Nguyen-Thanh, Phuong-Thao Nguyen-Vu, Quy-Anh Le-Thi, Thao-Nguyen Phan-Thi and Thi-Minh-Thi Ha
Curr. Issues Mol. Biol. 2024, 46(8), 8282-8300; https://doi.org/10.3390/cimb46080489 - 1 Aug 2024
Cited by 1 | Viewed by 1744
Abstract
The objective of this meta-analysis was to evaluate the association between maternal and fetal genetic variants and the risk of preeclampsia, a pregnancy-related condition that affects women. Despite the unclear role of these genetic factors in the development of preeclampsia, this analysis aimed [...] Read more.
The objective of this meta-analysis was to evaluate the association between maternal and fetal genetic variants and the risk of preeclampsia, a pregnancy-related condition that affects women. Despite the unclear role of these genetic factors in the development of preeclampsia, this analysis aimed to provide insights into the potential contributing factors. An electronic search of online databases was conducted to identify relevant studies. Stata SE software was used for the meta-analysis. A random-effects model was used to establish the association between the genetic variants and preeclampsia risk. Egger’s test was utilized to evaluate publication bias. Ten observational studies were selected from databases that met the inclusion criteria and included seven genes and twenty polymorphisms to analyze preeclampsia susceptibility influenced by the genetic background of both the mother and fetus. Our meta-analysis revealed that both the maternal and fetal polymorphisms, FLT1 rs4769613, were significantly associated with the risk of preeclampsia. However, the association between the maternal ACE rs4646994 polymorphism and preeclampsia risk was not statistically significant. Nevertheless, a significant association was observed between the fetal ACE rs4646994 polymorphism and preeclampsia in a dominant genetic model. In this study, the associations between maternal and fetal polymorphisms in ERAP2, VEGF, VDR, REN, and MMP were not statistically significant. According to the available evidence, maternal and fetal polymorphisms can impact the likelihood of developing preeclampsia. Additional research is required to fully understand the underlying mechanisms connecting maternal and fetal polymorphisms to preeclampsia, and to formulate recommendations for screening pregnant women based on these genetic variations. Full article
(This article belongs to the Special Issue Advanced Molecular Research on Hypertensive Disorders of Pregnancy (HDPs))
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Review

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15 pages, 956 KiB  
Review
Genetic Variations in Vascular Endothelial Growth Factor and Their Impact on Preeclampsia: Insights into Risk, Severity, and Pregnancy Outcomes
by Ioanna Zouganeli, Efthalia Moustakli, Anastasios Potiris, Chrysi Christodoulaki, Ioannis Arkoulis, Nikolaos Kathopoulis, Charalampos Theofanakis, Ekaterini Domali, Periklis Panagopoulos, Peter Drakakis and Sofoklis Stavros
Curr. Issues Mol. Biol. 2025, 47(3), 199; https://doi.org/10.3390/cimb47030199 - 17 Mar 2025
Viewed by 426
Abstract
Vascular endothelial growth factor (VEGF) plays a crucial role in angiogenesis and placental development, which are vital for a healthy pregnancy. Preeclampsia (PE), a hypertension condition that can cause major difficulties for both the mother and the fetus, has been linked to VEGF [...] Read more.
Vascular endothelial growth factor (VEGF) plays a crucial role in angiogenesis and placental development, which are vital for a healthy pregnancy. Preeclampsia (PE), a hypertension condition that can cause major difficulties for both the mother and the fetus, has been linked to VEGF gene polymorphisms in several studies. PE susceptibility has been associated with several VEGF polymorphisms, including VEGF −2578C/A, −634G/C, +936C/T, and +405G/C, with differing outcomes in various ethnicities. Some polymorphisms, like VEGF −2578C/A, are linked to the disease’s progression, whereas others, like VEGF +405G/C, may protect severe PE. The findings are still uncertain, though, with some studies reporting noteworthy outcomes and others finding no correlation. Further complicating our knowledge of VEGF’s role in PE is the possibility that the interaction between maternal and fetal VEGF polymorphisms may affect PE risk. Studies on environmental variables and placental and fetal VEGF gene polymorphisms point to a complicated interaction in influencing the severity and susceptibility of PE. The precise genetic processes behind PE are still unknown, despite the mounting evidence, necessitating additional research to confirm possible biomarkers and treatment targets. In at-risk pregnancies, a better understanding of the connection between VEGF polymorphisms and PE may help with risk assessment and management techniques. Full article
(This article belongs to the Special Issue Advanced Molecular Research on Hypertensive Disorders of Pregnancy (HDPs))
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Other

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10 pages, 1300 KiB  
Perspective
The Molecular Pathology of Pre-Eclamptic Hypertension
by Robin W. Carrell, Randy J. Read and Aiwu Zhou
Curr. Issues Mol. Biol. 2025, 47(5), 375; https://doi.org/10.3390/cimb47050375 - 20 May 2025
Abstract
The central role of angiotensinogen in the control of blood pressure is revealed by a series of crystallographic structures, including complexes with renin. Specifically, the structures provide an understanding of the sequential molecular events that lead to the pre-eclamptic hypertensive crises of pregnancy. [...] Read more.
The central role of angiotensinogen in the control of blood pressure is revealed by a series of crystallographic structures, including complexes with renin. Specifically, the structures provide an understanding of the sequential molecular events that lead to the pre-eclamptic hypertensive crises of pregnancy. The release of the precursor vasopressor peptide from the amino-terminal tail of angiotensinogen appears to be modulated by a redox-sensitive disulphide bridge. Our findings indicate that the activation of the thiol-switch in the circulating maternal angiotensinogen occurs at the placental level in response to oxidative stress, exacerbated by placental insufficiency. We propose here that a contributory factor is the inherent redox stress accompanying the placental exchange of oxygenation between the haemoglobin of the mother (oxy-HbA) and the deoxygenated haemoglobin of the foetus (deoxy-HbF). Full article
(This article belongs to the Special Issue Advanced Molecular Research on Hypertensive Disorders of Pregnancy (HDPs))
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