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Pathogenesis of Preeclampsia: From a Molecular Perspective
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Pathogenesis of Preeclampsia: From a Molecular Perspective

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 March 2026 | Viewed by 4109

Special Issue Editor

Dr. Jezid Miranda

E-Mail Website
Guest Editor
Department of Obstetrics and Gynecology, Faculty of Medicine, Universidad de Cartagena, Cartagena, Colombia
Interests: preeclampsia; immune system; molecular mechanisms in preeclampsia; angiogenic factors; gene regulation; epigenetics; transcription factors in preeclampsia; translational research in preeclampsia

Special Issue Information

Dear Colleagues,

Preeclampsia is a pregnancy-specific disorder characterized by placental malperfusion, significantly impacting maternal and perinatal health worldwide. Despite considerable research, its pathogenesis and etiology remain partially understood. This Special Issue focuses on the molecular aspects of preeclampsia, particularly its pathogenesis. We are interested in exploring the immune system’s role, specifically how immune maladaptation contributes to preeclampsia, and encouraging studies on immune responses in preeclamptic conditions. Additionally, we seek manuscripts addressing transcription and gene regulation in preeclampsia. Contributions that examine gene expression profiles, epigenetic changes, and regulatory pathways influencing gene expression linked to preeclampsia are particularly valued. This Special Issue also invites research integrating these molecular insights with translational research, aiming to close the gap between laboratory findings and clinical application.

By deepening our understanding of the molecular pathways involved in preeclampsia, we aim to enhance diagnostics, develop targeted therapies, and improve outcomes for mothers and infants. This Special Issue offers researchers and clinicians an opportunity to contribute to the evolving knowledge base on the complex molecular dynamics of preeclampsia. We eagerly anticipate your submissions and contributions to this important topic.

Dr. Jezid Miranda
Guest Editor

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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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • preeclampsia
  • immune system
  • molecular mechanisms in preeclampsia
  • angiogenic factors
  • gene regulation
  • epigenetics
  • transcription factors in preeclampsia
  • translational research in preeclampsia

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Published Papers (3 papers)

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Research

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11 pages, 1318 KB  
Article
Antibody-Dependent Cytotoxicity of Monocytes in Preeclampsia Is Associated with Soluble Forms of HLA
by Aleksey M. Krasnyi, Leya E. Sorokina, Anastacia Maria Argentova-Stevens, Diana N. Kokoeva, Aleksey A. Alekseev, Tatjana Jankevic, Natalia E. Kan, Victor L. Tyutyunnik and Gennady T. Sukhikh
Int. J. Mol. Sci. 2025, 26(23), 11638; https://doi.org/10.3390/ijms262311638 - 1 Dec 2025
Viewed by 337
Abstract
Preeclampsia (PE) is a serious gestational complication that affects the lives of the mother and the child. Women with PE showed higher levels of pro-inflammatory cytokines secreted by leukocytes compared with women with normal pregnancies. The differences are most noticeable in the percentage [...] Read more.
Preeclampsia (PE) is a serious gestational complication that affects the lives of the mother and the child. Women with PE showed higher levels of pro-inflammatory cytokines secreted by leukocytes compared with women with normal pregnancies. The differences are most noticeable in the percentage of CD16+ monocytes, although the mechanism underlying this increase remains unclear. The CD16 receptor is critical for antibody-dependent cellular cytotoxicity, and by binding to antibodies on the surface of target cells, it activates their death. In this study, we examined the effect of soluble placental factors on the expression of CD16 monocytes and the potential role the soluble form of human leukocyte antigen (HLA) has on CD16 monocyte expression. At the first stage of our study, we collected samples of placental villi fragments from 58 pregnant women (38 women with PE and 20 with a healthy pregnancy). Then we studied the effect of placental villus-conditioned culture medium on CD16 expression by monocytes derived from the same women. It was shown that the content of CD16+ monocytes increased significantly in women with PE within 3 h and to a lesser extent in women with a healthy pregnancy (p = 0.009). Also, the addition of the recombinant histocompatibility HLA-B to the placental villus-conditioned culture medium blocks the induction of CD16 expression on monocytes. At the second stage of our study, we typed HLA class I and class II alleles in the umbilical cord blood samples and the venous blood samples taken from 38 women with PE and 40 women with a normal pregnancy. It was found that certain HLA class II alleles predominate in women with preeclampsia. The DRB1*01:01:01G allele showed the greatest difference (p < 0.001). Analyzing five alleles simultaneously makes it possible to predict the PE with AUC = 0.76. Evaluation of unique children’s alleles also showed that class II alleles have greater differences among them than class I alleles. The DQB1*06:03:01G allele had the greatest differences with p = 0.03 (the number was higher in the control group). Performing an analysis of four alleles of children simultaneously allowed us to predict PE with an AUC of 0.64. This work suggests that the activation of CD16+ monocyte expression occurs due to the interaction of soluble placental antigens with monocytes. The most likely way to activate CD16 expression on monocytes is by HLA class II (both maternal and fetal) interaction with CD4 receptors on the surface of monocytes, whereas HLA class I is capable of blocking this process. Evaluation of maternal HLA alleles may be a significant marker for predicting PE. Full article
(This article belongs to the Special Issue Pathogenesis of Preeclampsia: From a Molecular Perspective)
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13 pages, 826 KB  
Article
Increased Preeclampsia Risk in GDM Pregnancies: The Role of SIRT1 rs12778366 Polymorphism and Telomere Length
by Olga Dmitrenko, Nataliia Karpova and Malik Nurbekov
Int. J. Mol. Sci. 2025, 26(7), 2967; https://doi.org/10.3390/ijms26072967 - 25 Mar 2025
Cited by 2 | Viewed by 1054
Abstract
Preeclampsia (PE) and gestational diabetes mellitus (GDM) are common pregnancy disorders with shared pathophysiological mechanisms. This study examined the association between SIRT1 polymorphisms (rs12778366 and rs7895833) and relative telomere length (RTL) in women with PE and GDM. The DNA from pregnant women with [...] Read more.
Preeclampsia (PE) and gestational diabetes mellitus (GDM) are common pregnancy disorders with shared pathophysiological mechanisms. This study examined the association between SIRT1 polymorphisms (rs12778366 and rs7895833) and relative telomere length (RTL) in women with PE and GDM. The DNA from pregnant women with GDM with and without PE was analyzed. The RTL and genotyping were measured using quantitative real-time PCR. The women with GDM and PE had significantly shorter telomeres. The rs12778366 TC genotype was associated with a 4.48-fold increased risk of PE (OR = 4.48; 95% CI 1.54–13.08; p = 0.003). The PE group had a higher prevalence of the heterozygous TC rs12778366 genotype with short telomeres. The SIRT1 variant rs12778366 is associated with shorter telomeres and an increased risk of developing preeclampsia, suggesting it may be a useful biomarker for preeclampsia risk assessment in GDM pregnancies. Full article
(This article belongs to the Special Issue Pathogenesis of Preeclampsia: From a Molecular Perspective)
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Review

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35 pages, 5011 KB  
Review
A Disintegrin and Metalloprotease with Thrombospondin Motif, Member 13, and Von Willebrand Factor in Relation to the Duality of Preeclampsia and HIV Infection
by Prelene Naidoo and Thajasvarie Naicker
Int. J. Mol. Sci. 2025, 26(9), 4103; https://doi.org/10.3390/ijms26094103 - 25 Apr 2025
Viewed by 1594
Abstract
Normal pregnancy is associated with multiple changes in the coagulation and the fibrinolytic system. In contrast to a non-pregnant state, pregnancy is a hypercoagulable state where the level of VWF increases by 200–375%, affecting coagulation activity. Moreover, in this hypercoagulable state of pregnancy, [...] Read more.
Normal pregnancy is associated with multiple changes in the coagulation and the fibrinolytic system. In contrast to a non-pregnant state, pregnancy is a hypercoagulable state where the level of VWF increases by 200–375%, affecting coagulation activity. Moreover, in this hypercoagulable state of pregnancy, preeclampsia is exacerbated. ADAMTS13 cleaves the bond between Tyr1605 and Met1606 in the A2 domain of VWF, thereby reducing its molecular weight. A deficiency of ADAMTS13 originates from mutations in gene or autoantibodies formed against the protease, leading to defective enzyme production. Von Willebrand protein is critical for hemostasis and thrombosis, promoting thrombus formation by mediating the adhesion of platelets and aggregation at high shear stress conditions within the vessel wall. Mutations in VWF disrupts multimer assembly, secretion and/or catabolism, thereby influencing bleeding. VWF is the primary regulator of plasma ADAMTS13 levels since even minute amounts of active ADAMTS13 protease have a significant inhibitory effect on inflammation and thrombosis. VWF is released as a result of endothelial activation brought on by HIV infection. The SARS-CoV-2 infection promotes circulating proinflammatory cytokines, increasing endothelial secretion of ultra large VWF that causes an imbalance in VWF/ADAMTS13. Raised VWF levels corresponds with greater platelet adhesiveness, promoting a thrombotic tendency in stenotic vessels, leading to increased shear stress conditions. Full article
(This article belongs to the Special Issue Pathogenesis of Preeclampsia: From a Molecular Perspective)
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