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Common Mechanisms in Gestational Diabetes, Preeclampsia, and Coronavirus Disease 2019

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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: 30 September 2026 | Viewed by 24536

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Dr. Sandor G. Vari

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International Research and Innovation in Medicine Program, Cedars–Sinai Medical Center, Los Angeles, CA 90048, USA
Interests: gestational diabetes; preeclampsia; inflammation; immunoglobulins; glycolisation; platelet aggregation; microvascular thrombosis; COVID-19

Special Issue Information

Dear Colleagues,

The leading cause of changes in the placenta is inflammation that is characterized by immunoglobulins, C-reactive protein, interleukins, and cytokines TNF-α and IFN-γ, as well as decidual cytokine IL-32.

We are pleased to invite you to present your results in the field of low-grade inflammation, immunoglobulins, glycolisation, platelet aggregation, and microvascular thrombosis. Inflammation induces tissue damage that can be measured with inflammation markers, immunoglobulins, glycolisation, platelet aggregation, and microvascular thrombosis.

The pro-angiogenic effects on the fetoplacental circulation support trophoblast growth, and placental angiogenesis will be monitored by measuring serum vascular endothelial growth factor (VEGF), Annexin A2, and placental growth factor (PGF). Also, it is required to investigate umbilical cord plasma sclerostin as a predictor of placental and newborn weight.

Suggested themes and article types for submissions: original research (brief reports, research letters), review articles (narrative, systematic, meta-analysis, clinical practice, epidemiology), case reports, and methodology articles.

Research areas may include (but are not limited to) the following:

A high-risk pregnancy.
Hormonal and physiological changes that cause insulin resistance in GDM.
Gestational hypertension, preeclampsia, and eclampsia in coronavirus disease 2019.
Low-grade inflammation.
Glycolisation of immunoglobulins during GDM, PE, and COVID-19.
Placental angiogenesis.
Change in platelet aggregation during pregnancy.
Change in mother milk composition due to nutritional factors in GDM and PE.

We look forward to receiving your contributions.

Dr. Sandor G. Vari
Guest Editor

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Keywords

gestational diabetes
preeclampsia
inflammation
immunoglobulins
glycolisation
platelet aggregation
microvascular thrombosis
coronavirus disease 2019

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Published Papers (10 papers)

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Research

Jump to: Review

13 pages, 2772 KB

Open AccessArticle

SARS-CoV-2 Infection Exacerbates Hypertensive Disorders in Pregnancy Through Vascular and Immune Pathways

by Marta Fabre, Ana Medel-Martinez, Pilar Calvo, Natalia Abadia-Cuchi, Sara Ruiz-Martinez, Maria Peran, Cristina Paules, Alberto Montolío, Beatriz Jimeno-Beltrán, Javier Godino, Alberto Cebollada-Solanas, Mark Strunk, Fatima Crispi, Daniel Oros and Jon Schoorlemmer

Int. J. Mol. Sci. 2026, 27(13), 5891; https://doi.org/10.3390/ijms27135891 - 30 Jun 2026

Viewed by 360

Abstract

Background: SARS-CoV-2 infection has been linked to an increased risk of hypertensive disorders during pregnancy, particularly preeclampsia (PE). As both conditions involve vascular and endothelial dysfunction, a mechanistic overlap has been proposed. This study examines the relationship between maternal COVID-19 and preeclampsia by analyzing inflammatory, endothelial, and angiogenic biomarkers in pregnancies with and without these complications. Methods: A case–control study was conducted, including four groups: healthy pregnancies before 2020 (n = 10), preeclampsia cases before 2020 (n = 10), COVID-19 cases without preeclampsia (n = 10), and COVID-19 cases with preeclampsia (n = 10). The groups were selected to be comparable in terms of gestational age at blood sampling. Biomarkers related to endothelial, inflammatory, and angiogenic pathways were measured. Results: Significant differences in biomarker levels were detected among the four groups. Regarding endothelial damage, sICAM1 levels were significantly higher in the COVID-PE group compared with the COVID-noPE group (p = 0.002). Additionally, vWF (p = 0.006), END1 (p < 0.001), and sVCAM1 (p = 0.030) levels varied significantly across groups. IL8 levels showed significant differences (p < 0.001), and were particularly elevated in preeclampsia cases (preCOVID-PE and COVID-PE groups) compared with controls (p = 0.005 and p < 0.001, respectively). Angiogenic markers sFlt-1, PLGF, and sFlt-1/PLGF exhibited significant group differences (p < 0.001). In contrast, maternal SARS-CoV-2 infection in the absence of preeclampsia was not associated with a significant alteration of the sFlt-1/PlGF ratio. Discussion: PE associated with SARS-CoV-2 infection preserved the classical angiogenic signature of preeclampsia, but showed additional endothelial and inflammatory biomarker alterations. These findings support an association between SARS-CoV-2 infection and a distinct endothelial and inflammatory biomarker profile in PE, warranting confirmation in larger prospective studies. Full article

(This article belongs to the Special Issue Common Mechanisms in Gestational Diabetes, Preeclampsia, and Coronavirus Disease 2019)

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16 pages, 638 KB

Open AccessArticle

NRF2 Gene Polymorphisms, Preconception BMI and Their Interplay in Preeclampsia

by Ziye Li, Suyan Guo, Xuan Zhou, Junxiang Miao, Fan Xia, Lizhang Chen and Tingting Wang

Int. J. Mol. Sci. 2026, 27(13), 5705; https://doi.org/10.3390/ijms27135705 - 24 Jun 2026

Viewed by 317

Abstract

This study aimed to explore the correlations of nuclear factor erythroid 2-related factor-2 (NRF2) gene polymorphisms, prepregnancy body mass index (BMI) and the interaction between them with the risk of preeclampsia (PE). A case–control study was conducted in which pregnant women with PE (n = 198) and normotensive pregnant women (n = 396) were recruited as the case group and control group, respectively, from two tertiary hospitals in Hunan Province. Data collection was achieved through face-to-face interviews utilizing a standardized questionnaire, along with perinatal health care records. Blood samples were also collected, and genotyping of nine single-nucleotide polymorphisms (SNPs) in the NRF2 gene was subsequently performed using the MassArray platform. Both univariate and multivariate logistic regression analyses were employed to assess the associations of NRF2 gene polymorphisms with prepregnancy BMI and their interactions with the risk of PE. Multivariate logistic regression analyses revealed a significant association between prepregnancy BMI and PE susceptibility. Specifically, prepregnancy overweight/obesity (BMI ≥ 24.0 kg/m²) was associated with an elevated risk of PE (adjusted OR = 4.59, 95% CI: 2.82–7.45), whereas underweight status (BMI < 18.5 kg/m²) was correlated with a reduced PE risk (adjusted OR = 0.38, 95% CI: 0.18–0.78). The NRF2 polymorphism rs13005431 exhibited a protective effect against PE under the additive genetic model (adjusted OR = 0.59, 95% CI: 0.37–0.93). Furthermore, logistic regression analyses revealed a significant effect of the multiplicative interaction between prepregnancy overweight/obesity and polymorphisms rs35652124 (adjusted OR = 0.24, 95% CI: 0.06–0.89) and rs2627765 (adjusted OR = 3.62, 95% CI: 1.07–12.23) on susceptibility to PE. These findings collectively underscore the critical and independent roles of prepregnancy BMI, NRF2 polymorphisms, and their interactions in modulating PE susceptibility, suggesting that the combined effects of metabolic profiles and genetic determinants may act synergistically to shape PE risk. Full article

(This article belongs to the Special Issue Common Mechanisms in Gestational Diabetes, Preeclampsia, and Coronavirus Disease 2019)

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19 pages, 2740 KB

Open AccessArticle

IgG N-Glycan Profiles in Mothers and Infants Postpartum in the Context of Maternal Obesity and Gestational Diabetes

by Anna Farkas, Oksana Matsyura, Lesya Besh, Andras Guttman and Sandor G. Vari

Int. J. Mol. Sci. 2025, 26(21), 10641; https://doi.org/10.3390/ijms262110641 - 31 Oct 2025

Cited by 2 | Viewed by 1002

Abstract

This study explored IgG N-glycosylation pattern differences in maternal and infant serum in the context of gestational diabetes mellitus (GDM). Serum samples from 15 mother–infant pairs were collected at 12 weeks postpartum and categorized according to maternal body mass index (BMI) and GDM status. The N-glycosylation patterns of the isolated IgG pools were analyzed by capillary electrophoresis with laser-induced fluorescence detection (CE-LIF). Descriptive comparison of the relative area percentage of IgG N-glycan structures revealed differences between the groups. Comparison of the maternal and infant sialo-form/neutral-form ratio (SF/NF) of the N-glycans suggested differences between control mothers and their children, as well as between obese mothers and their children. The maternal SF/NF ratio of IgG varied between the obese and normal-weight GDM mothers. The SF/NF ratios of IgG from the infants showed variation between infants of control mothers and infants of obese mothers, between infants of obese and infants of obese GDM mothers, and between infants of GDM with normal-weight and GDM with obese mothers. The observed differences in maternal and infant IgG N-glycosylation profiles suggest potentially selective placental transfer mechanisms. Full article

(This article belongs to the Special Issue Common Mechanisms in Gestational Diabetes, Preeclampsia, and Coronavirus Disease 2019)

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20 pages, 3845 KB

Open AccessArticle

Vaping in Pregnancy: Unraveling Molecular Drivers of Preeclampsia and Fetal Growth Restriction

by Archarlie Chou, Olivia Hiatt, Benjamin Davidson, Paul R. Reynolds, Brett E. Pickett and Juan A. Arroyo

Int. J. Mol. Sci. 2025, 26(20), 10009; https://doi.org/10.3390/ijms262010009 - 15 Oct 2025

Cited by 1 | Viewed by 2386

Abstract

Preeclampsia (PE) and intrauterine growth restriction (IUGR) are major pregnancy complications that are linked to placental dysfunction and environmental stimulation such as the use of electronic cigarettes (eCig). This study investigates the molecular impacts of timed eCig exposure in a C57BL/6 mouse model of PE and IUGR using bulk RNA-sequencing of placental tissues. Pregnant mice were exposed to eCig vapor via nose-only system starting at embryonic day 12.5 (eCig-6d, before spiral artery (SA) invasion) or 14.5 (eCig-4d, after SA invasion) until E18.5 (necropsy), with healthy controls exposed to room air (n = 6/group). The eCig-4d group developed PE, whereas the eCig-6d group developed both PE and IUGR. RNA-seq analysis revealed 429 differentially expressed genes (DEGs) in eCig-4d (IUGR-like) group and 64 DEGs in eCig-6d (PE + IUGR-like) group compared to controls. Pathway and gene network analyses indicated that eCig-4d exposure activated NF-κB–driven inflammation, suppressed ECM organization and collagen biosynthesis, and downregulated vasoactive genes/mitochondrial-associated genes (NOS1/2), accompanied by impaired complement initiation and reduced both macrophage and monocyte signals. Similarly, eCig-6d exposure led to downregulation of complement-associated genes and granule-related components, possibly implicating weakened neutrophil responsiveness and compromised inflammatory resolution at the maternal–fetal interface. Our findings align with prior studies on physiological dysfunctions in PE and IUGR, while also providing novel insights into the temporally specific cellular responses induced by eCig exposure. Full article

(This article belongs to the Special Issue Common Mechanisms in Gestational Diabetes, Preeclampsia, and Coronavirus Disease 2019)

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14 pages, 1466 KB

Open AccessArticle

Placental Dysfunction Is Associated with Dysregulated Fibrinolytic System Activation

by Tetiana Yatsenko, Iryna Us, Daria Korolova, Svitlana Zhuk, Halyna Dziuba, Alona Nalbat, Svitlana Kharchenko, Sandor George Vari and Volodymyr Chernyshenko

Int. J. Mol. Sci. 2025, 26(19), 9339; https://doi.org/10.3390/ijms26199339 - 24 Sep 2025

Cited by 6 | Viewed by 1758

Abstract

During pregnancy, the maternal hemostatic system undergoes significant changes to support placental angiogenesis, maintain fetal blood flow, and ensure safe delivery. This study investigates the dysregulation of hemostasis in placental insufficiency and explores potential markers for diagnosing and managing this gestational complication. Thromboelastography, coagulation and fibrinolysis functional assays, ELISA, and immunoblotting were employed to assess hemostasis dysregulation in placental dysfunction of two cohorts of pregnant women with placental dysfunction and healthy controls. Thromboelastographic analysis revealed no significant differences in clot lysis indices between the control and placental dysfunction groups, with values remaining within normal ranges, suggesting this method’s limitations for assessing fibrinolysis in pregnancy. The placental dysfunction group demonstrated moderately increased fibrinogen levels and platelet sensitivity to ADP, indicating hemostasis reactiveness. Significantly lower D-dimer levels, decreased plasminogen activator inhibitor activity (total PAI-1 + PAI-2), and increased plasminogen activator activity, driven primarily by uPA in the placental dysfunction group, indicated abnormal fibrinolysis. Immunoblotting confirmed elevated uPA/uPA-PAI complexes and reduced tPA/tPA-PAI complexes, indicating that shutdown of tPA-mediated fibrinolysis and induction of uPA-driven vessel-wall-associated proteolysis are linked to placental dysfunction. Placental dysfunction involves fibrinolytic system dysregulation, marked by decreased PAI and tPA, uPA overproduction, and hypofibrinolysis, contributing to thrombotic risks, impaired placental flow, and complications like fetal growth retardation. PAI/PA ratio and D-dimer levels have diagnostic potential for placental-dysfunction-associated complications. Full article

(This article belongs to the Special Issue Common Mechanisms in Gestational Diabetes, Preeclampsia, and Coronavirus Disease 2019)

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17 pages, 5398 KB

Open AccessArticle

Changes in Placentas of Pregnant Women Infected with COVID-19

by Solomiia Kramar, Zoia Nebesna, Yuliia Yakymchuk, Alla Boychuk, Oksana Shevchuk, Mykhaylo Korda and Sandor George Vari

Int. J. Mol. Sci. 2025, 26(17), 8596; https://doi.org/10.3390/ijms26178596 - 4 Sep 2025

Cited by 6 | Viewed by 2873

Abstract

SARS-CoV-2 infection in pregnant women can lead to pregnancy-related complications. This work aims to study the spectrum of pathological changes in the placentas of SARS-CoV-2-infected pregnant women. The study involved 50 pregnant women with COVID-19 disease in the first (group I), second (group II), and third (group III) trimesters. Placental sections were examined by histopathology, electron microscopy, and immunohistochemistry to assess structural and molecular changes. The placentas of SARS-CoV-2-affected pregnant women exhibit nonspecific pathological changes, primarily associated with impaired blood circulation. The most frequent findings include thrombosis, chorangiosis, villous edema, and fibrinoid necrosis, all indicative of endothelial dysfunction. Increased expression of sclerostin and Annexin A2 was also detected in affected placentas. The main submicroscopic manifestations of placental insufficiency in COVID-19-affected women are dystrophic–destructive changes in the stroma of the villi, manifested by edema and fibrous processes, which cause significant disruption of the fetoplacental barrier. SARS-CoV-2 causes thrombotic and sclerotic changes, mainly in the maternal portion of the placenta. The manifestation of pathological changes in the placenta of COVID-19-affected women depends on the pregnancy period during which infection by SARS-CoV-2 has occurred. The established findings may provide insights into the connection between COVID-19 in pregnancy and antenatal and perinatal outcomes. Full article

(This article belongs to the Special Issue Common Mechanisms in Gestational Diabetes, Preeclampsia, and Coronavirus Disease 2019)

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Review

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36 pages, 3267 KB

Open AccessReview

Metabolic Reprogramming at the Maternal–Fetal Interface: Insights from Decidual Stromal Cells and Trophoblasts in Healthy Pregnancy Versus Recurrent Pregnancy Loss

by Zhuo Liu, Zhuo Zhang, Yanjing Huang, Fan Li, Yuli Geng, Runan Hu, Mingmin Zhang and Yufan Song

Int. J. Mol. Sci. 2026, 27(14), 6413; https://doi.org/10.3390/ijms27146413 - 19 Jul 2026

Viewed by 702

Abstract

Metabolic reprogramming at the maternal–fetal interface remodels enzymes, metabolites, and pathways to orchestrate decidualization, placentation, and immune tolerance, thereby sustaining cellular homeostasis and maternal-fetal adaptation. Disruption of this precisely coordinated metabolic reprogramming impairs these processes, contributing to recurrent pregnancy loss (RPL). This review focuses on the two most abundant cell types at the maternal–fetal interface: maternal-derived decidual stromal cells (DSCs) and embryo-derived trophoblasts, and systematically delineates their metabolic reprogramming in healthy pregnancy versus RPL. Recent advances reveal that altered glucose, lipid, amino acid, redox, and one-carbon metabolism in DSCs and trophoblasts drives defective decidualization, placentation, and immune tolerance, offering novel mechanistic insights into RPL etiology. These findings highlight potential metabolic biomarkers and therapeutic strategies, bridging mechanistic discoveries with translational opportunities for RPL. Full article

(This article belongs to the Special Issue Common Mechanisms in Gestational Diabetes, Preeclampsia, and Coronavirus Disease 2019)

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16 pages, 1337 KB

Open AccessReview

The Placenta–Gut Microbiota Axis in Gestational Diabetes Mellitus: Molecular Mechanisms, Crosstalk, and Therapeutic Perspectives

by Reka Anna Vass, Eva Miko, Viktoria Premusz, Sandor G. Vari, Kalman Kovacs, Jozsef Bodis and Tibor Ertl

Int. J. Mol. Sci. 2026, 27(1), 312; https://doi.org/10.3390/ijms27010312 - 27 Dec 2025

Cited by 4 | Viewed by 2083

Abstract

Gestational diabetes mellitus (GDM) is a multifactorial metabolic disorder arising from impaired insulin sensitivity and altered maternal–fetal energy regulation. Beyond classical mechanisms involving β-cell dysfunction and pregnancy-induced insulin resistance, emerging evidence suggests a bidirectional interaction between the maternal gut microbiota and the placenta, forming a dynamic placenta–gut axis. Microbial dysbiosis alters levels of metabolites, inflammatory mediators, and bile acids, which influence placental signaling, trophoblast metabolism, immune activation, and nutrient transport. Conversely, the placenta secretes hormones, cytokines, lipids, and exosomal miRNAs that shape maternal metabolism and potentially modulate the gut microbiota. This review synthesizes current mechanistic insights underlying the placenta–gut microbiota axis in GDM, describes immune and metabolic crosstalk, and highlights therapeutic opportunities targeting this inter-organ communication system. Addressing these interactions may advance precision strategies for managing GDM and improving outcomes across generations. Full article

(This article belongs to the Special Issue Common Mechanisms in Gestational Diabetes, Preeclampsia, and Coronavirus Disease 2019)

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22 pages, 929 KB

Open AccessReview

Late vs. Early Preeclampsia

by Maria Kariori, Vasiliki Katsi and Costas Tsioufis

Int. J. Mol. Sci. 2025, 26(22), 11091; https://doi.org/10.3390/ijms262211091 - 16 Nov 2025

Cited by 22 | Viewed by 5535

Abstract

Preeclampsia (PE) is a complex hypertensive disorder of pregnancy characterized by new-onset hypertension and proteinuria after 20 weeks of gestation. It is classified into early-onset (EOPE, <34 weeks) and late-onset (LOPE, ≥34 weeks) subtypes, which differ in their pathophysiology, clinical course, and maternal and neonatal outcomes. EOPE arises from abnormal placentation with inadequate spiral artery remodeling and impaired uteroplacental perfusion, whereas LOPE is mainly related to maternal cardiovascular and metabolic predisposition. This review integrates current molecular, immunological, and hemodynamic evidence distinguishing EOPE from LOPE, emphasizing recent insights into angiogenic imbalance (VEGF, PlGF, sFlt-1), oxidative stress, and immune modulation. It also summarizes evolving diagnostic and prognostic biomarkers and evaluates emerging therapeutic approaches, including gene therapy targeting placental dysfunction. By comparing mechanistic pathways and clinical implications, this review highlights how gestational age–specific pathogenesis may inform risk stratification, early detection, and precision-based management of PE. Full article

(This article belongs to the Special Issue Common Mechanisms in Gestational Diabetes, Preeclampsia, and Coronavirus Disease 2019)

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24 pages, 1057 KB

Open AccessReview

The Role of Angiogenetic Factors in Preeclampsia

by Angeliki Papapanagiotou, Maria Anastasia Daskalaki, Antonios N. Gargalionis, Angeliki Margoni, Aikaterini Domali, George Daskalakis and Athanasios G. Papavassiliou

Int. J. Mol. Sci. 2025, 26(21), 10431; https://doi.org/10.3390/ijms262110431 - 27 Oct 2025

Cited by 17 | Viewed by 5905

Abstract

Preeclampsia (PE) occurs in approximately 2–8% of all pregnancies worldwide and represents one of the primary causes of maternal and fetal morbidity and mortality. Angiogenic growth factors such as placental growth factor (PlGF) and vascular endothelial growth factor (VEGF), along with their tyrosine kinase receptor (Flt-1), play a central role in placental and fetal development. Impaired placentation results in the excessive release of the antiangiogenic soluble fms-like tyrosine kinase-1 (sFlt-1) which is pivotal in the pathogenesis of PE. By binding to and neutralizing angiogenic factors, sFlt-1 disrupts normal angiogenic signaling, creating an imbalance that is often detectable before clinical symptoms of PE appear. Recent studies have highlighted the prognostic potential of the sFlt-1/PlGf ratio as an early indicator of PE risk, since this ratio has demonstrated value in both confirming and excluding PE in the high-risk population. Its incorporation into routine medical care has the potential to reduce unnecessary hospital admissions, intensive management, and premature deliveries, ultimately lowering healthcare costs. The objective of this review is to highlight the clinical utility of the sFlt-1/PlGf ratio in the prediction, diagnosis, and management of preeclampsia and to emphasize the cost-effectiveness of implementing sFlt-1/PlGF ratio measurement in the care of women at risk of developing PE. Full article

(This article belongs to the Special Issue Common Mechanisms in Gestational Diabetes, Preeclampsia, and Coronavirus Disease 2019)

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