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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 August 2025 | Viewed by 1391

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

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

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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
  • 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 (2 papers)

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13 pages, 826 KiB  
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
Viewed by 231
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 KiB  
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 269
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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