Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (580 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A complication of pregnancy, characterized by a complex of symptoms including maternal hypertension and proteinuria with or without pathological edema. Symptoms may range between mild and severe. Pre-eclampsia usually occurs after the 20th week of gestation, but may develop before this time in the presence of trophoblastic disease.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Pre Eclampsia; Preeclampsia; Pregnancy Toxemias; Pregnancy Toxemia; Toxemia, Pregnancy; Edema-Proteinuria-Hypertension Gestosis; Edema Proteinuria Hypertension Gestosis; Gestosis, Edema-Proteinuria-Hypertension.
Where it fits in the MeSH classification
- Broader topics
- Hypertension, Pregnancy-Induced
- See also
- Toxemia
Related concepts
- Pregnancy
- Hypertension
- Proteinuria
- Edema
Research landscape
PubMed indexes 40,423 records tagged with the MeSH heading “Pre-Eclampsia” (counts retrieved 2026-11-04). 9,657 of them (23.9%) were published from 2020 onward, and the busiest period so far is through 1999 with 14,074 records.
Reviews account for 5,548 records (13.7%) and meta-analyses for 823. Randomized controlled trials number 760 (1.9%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 14,074 |
| 2000-2009 | 6,070 |
| 2010-2019 | 10,622 |
| 2020 onward | 9,657 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 5,548 | 13.7% |
| Meta-analyses | 823 | 2.0% |
| Randomized controlled trials | 760 | 1.9% |
Method: PubMed query "Pre-Eclampsia"[MeSH Terms] with publication-type and date filters, retrieved 2026-11-04.
Reading the evidence in kidney, urology and women's health
Kidney, urinary and reproductive health research uses lab markers (such as creatinine), imaging, symptom scores and registry data on pregnancy and birth. Findings about pregnancy are especially sensitive to who was studied and when in pregnancy exposure occurred. Nothing on this page is advice about treatment, fertility or pregnancy; speak to a qualified clinician. Check the population, the outcome measured and whether the study accounted for other health differences between groups.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Immune Cells in Preeclampsia | 2025 | Review article Design not recorded in structured metadata | 4 | cc by PMID 41515952 · DOI · PMC12785759 |
| Maternal causation of early-onset pre-eclampsia: excessive endometrial gland-derived apolipoprotein D induces placental ferroptosis and developmental abnormalities | 2025 | Research article Design not recorded in structured metadata | 4 | cc by PMID 41366770 · DOI · PMC12690863 |
| Defective Trophoblast Differentiation, Endothelial Dysfunction, and Immune Dysregulation in Preeclampsia Coalesce on a Placental VGLL3-Centered Gene Network | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 41953989 · DOI · PMC13120743 |
Immune Cells in Preeclampsia [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Preeclampsia (PE), new-onset hypertension during pregnancy, is associated with chronic inflammation both in the placenta and systemically.
- Closing excerpt
- As the immune system plays a role in the pathophysiology of the disease, it may be a potential target for therapeutic intervention to improve maternal and fetal outcomes during and following a PE pregnancy.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (190 words)
Preeclampsia (PE), new-onset hypertension during pregnancy, is associated with chronic inflammation both in the placenta and systemically. PE is characterized by placental ischemia, which then results in the production and release of anti-angiogenic factors and inflammatory mediators. Inflammation in PE leads to placental, renal, and vascular damage, which contribute to the phenotype of hypertension and organ dysfunction during pregnancy. T cells, B cells, Natural Killer cells, and macrophages have all been shown to play a role in the inflammation present in the disease. T helper cells contribute to the chronic inflammation in PE. They also activate B cells, which produce agonistic autoantibodies against the angiotensin II type 1 receptor. Natural Killer cells are activated in PE and shift away from decidual Natural killer cells, which produce angiogenic factors, and toward cytotoxic Natural Killer cells, which contribute to tissue damage. Macrophages are polarized towards proinflammatory subtypes and contribute to tissue damage and inflammatory signaling in PE patients. As the immune system plays a role in the pathophysiology of the disease, it may be a potential target for therapeutic intervention to improve maternal and fetal outcomes during and following a PE pregnancy.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41515952 · DOI · PMC12785759
Maternal causation of early-onset pre-eclampsia: excessive endometrial gland-derived apolipoprotein D induces placental ferroptosis and developmental abnormalities [2]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundEarly-onset pre-eclampsia (ePE) is a severe pregnancy complication characterized by dysregulated trophoblast functions and impaired placentation during early pregnancy, leading to substantial maternal and fetal morbidity.
- Closing excerpt
- APOD was identified as a crucial endometrial gland-secreted factor contributing to ePE, suggesting its potential as an early biomarker and therapeutic target.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (234 words)
BackgroundEarly-onset pre-eclampsia (ePE) is a severe pregnancy complication characterized by dysregulated trophoblast functions and impaired placentation during early pregnancy, leading to substantial maternal and fetal morbidity. While circumstantial evidence indicates defective secretion from endometrial glands impairs placental development, direct evidence linking maternal glandular dysfunction to ePE pathogenesis remains elusive.MethodsWe established endometrial glandular organoids from women with ePE and healthy pregnancies, analyzing their secretomes by iTRAQ-based proteomics, RNAseq, and spatial transcriptomics. Functional effects of organoid secretomes on trophoblasts were examined in vitro. An endometrial-specific apolipoprotein D (APOD) knock-in mouse model was studied in vivo. APOD levels in first-trimester serum samples from women who later developed ePE were compared to healthy pregnancies.ResultsSecretomes from ePE derived endometrial organoids impeded spiral artery remodeling. Multiomic analyses revealed increased APOD production in both ePE organoids and decidual tissues. APOD overexpression disrupted trophoblast functions and endothelial vascular remodeling in vitro, and recapitulated ePE phenotypes in an APOD knock-in mouse model through PI3K/Akt-mediated placental ferroptosis and potential ER stress induction. Ferroptosis inhibition with Fer-1 rescued placental defects and PE symptoms in APOD knock-in mice. Elevated APOD levels in first-trimester serum samples from women who later developed ePE suggest its potential as an early biomarker.ConclusionThis study provides the first direct evidence linking dysregulated endometrial gland function to defective placentation and ePE. APOD was identified as a crucial endometrial gland-secreted factor contributing to ePE, suggesting its potential as an early biomarker and therapeutic target.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41366770 · DOI · PMC12690863
Defective Trophoblast Differentiation, Endothelial Dysfunction, and Immune Dysregulation in Preeclampsia Coalesce on a Placental VGLL3-Centered Gene Network [3]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundPreeclampsia affects approximately 1 in 10 pregnancies, leading to severe complications and long-term health risks for both mother and offspring.
- Closing excerpt
- ConclusionsThese findings position VGLL3 as a promising novel therapeutic target for preeclampsia.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (156 words)
BackgroundPreeclampsia affects approximately 1 in 10 pregnancies, leading to severe complications and long-term health risks for both mother and offspring. While the etiology remains unclear, preeclampsia has been linked to both autoimmunity and the timing of menarche.MethodsThrough human single-cell and spatial analyses, coupled with in vitro, in vivo, and ex vivo models, we demonstrate that VGLL3 (Vestigial-like family member 3), a transcription coregulator in the Hippo pathway, is upregulated in preeclamptic placentas.ResultsVGLL3 promotes immune activation, impairs trophoblast differentiation, and induces endothelial dysfunction, all of which contribute to pregnancy-related hypertension, fetal growth restriction, and offspring mortality. Our data reveal that VGLL3 acts upstream of preeclampsia-associated processes, including the production of sFLT1 (soluble fms-like tyrosine kinase 1), a key biomarker of the disease. Notably, targeting VGLL3, either by genetic deletion in mouse placentas or through therapeutic inhibition in human placentas, protects against preeclampsia and alleviates disease pathology.ConclusionsThese findings position VGLL3 as a promising novel therapeutic target for preeclampsia.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41953989 · DOI · PMC13120743
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Preeclampsia and Future Cardiovascular Health: A Systematic Review and Meta-Analysis [4]
- Research article Clinical risk factors for pre-eclampsia determined in early pregnancy: systematic review and meta-analysis of large cohort studies [5]
- Research article The impact of COVID-19 on pregnancy outcomes: a systematic review and meta-analysis [6]
- Research article The role of aspirin dose on the prevention of preeclampsia and fetal growth restriction: systematic review and meta-analysis [7]
- Research article Association between gut microbiota and preeclampsia-eclampsia: a two-sample Mendelian randomization study [8]
- Research article Omega-3 fatty acid addition during pregnancy [9]
Full-text reviews on EvidenceLib
Open-access review articles about this topic, reproduced in full with authors, licence and references.
A Narrative Review on the Pathophysiology of Preeclampsia
Johnatan Torres-Torres, Salvador Espino-y-Sosa, Raigam Martinez-Portilla et al. · International Journal of Molecular Sciences 2024 · CC BY 4.0
Dose of aspirin to prevent preterm preeclampsia in women with moderate or high-risk factors: A systematic review and meta-analysis
Rachel Van Doorn, Narmin Mukhtarova, Ian P. Flyke et al. · PLoS ONE 2021 · CC BY 4.0
Systematic review of prediction models for gestational hypertension and preeclampsia
Edward Antwi, Mary Amoakoh-Coleman, Dorice L Vieira et al. · PLoS ONE 2020 · CC0 1.0
Systematic and meta-analysis of factors associated with preeclampsia and eclampsia in sub-Saharan Africa
Maereg Wagnew Meazaw, Catherine Chojenta, Muluken Dessalegn Muluneh et al. · PLoS ONE 2020 · CC BY 4.0
Assisted reproductive technology and the risk of preeclampsia: an updated systematic review and meta-analysis
Amir Almasi-Hashiani, Reza Omani-Samani, Maryam Mohammadi et al. · BMC Pregnancy and Childbirth 2019 · CC BY 4.0
References
- Campbell N, Robbins M, Nembaware H, Deer E, Cornelius D, LaMarca B. Immune Cells in Preeclampsia. . 2025. PMID 41515952 · DOI · PMC12785759
- Dong Y, Lee CL, Li J, Liu X, Zeng Q, Zhong J, et al.. Maternal causation of early-onset pre-eclampsia: excessive endometrial gland-derived apolipoprotein D induces placental ferroptosis and developmental abnormalities. . 2025. PMID 41366770 · DOI · PMC12690863
- Plazyo O, Chopp LB, Peela R, Young K, Zhang H, Bogle R, et al.. Defective Trophoblast Differentiation, Endothelial Dysfunction, and Immune Dysregulation in Preeclampsia Coalesce on a Placental VGLL3-Centered Gene Network. . 2026. PMID 41953989 · DOI · PMC13120743
- Wu P, Haththotuwa R, Kwok CS, Babu A, Kotronias RA, Rushton C, et al.. Preeclampsia and Future Cardiovascular Health: A Systematic Review and Meta-Analysis. Circ Cardiovasc Qual Outcomes. 2017. PMID 28228456 · DOI
- Bartsch E, Medcalf KE, Park AL, Ray JG, High Risk of Pre-eclampsia Identification Group. Clinical risk factors for pre-eclampsia determined in early pregnancy: systematic review and meta-analysis of large cohort studies. BMJ. 2016. PMID 27094586 · DOI · PMC4837230
- Wei SQ, Bilodeau-Bertrand M, Liu S, Auger N. The impact of COVID-19 on pregnancy outcomes: a systematic review and meta-analysis. CMAJ. 2021. PMID 33741725 · DOI · PMC8084555
- Roberge S, Nicolaides K, Demers S, Hyett J, Chaillet N, Bujold E. The role of aspirin dose on the prevention of preeclampsia and fetal growth restriction: systematic review and meta-analysis. Am J Obstet Gynecol. 2017. PMID 27640943 · DOI
- Li P, Wang H, Guo L, Gou X, Chen G, Lin D, et al.. Association between gut microbiota and preeclampsia-eclampsia: a two-sample Mendelian randomization study. BMC Med. 2022. PMID 36380372 · DOI · PMC9667679
- Middleton P, Gomersall JC, Gould JF, Shepherd E, Olsen SF, Makrides M. Omega-3 fatty acid addition during pregnancy. Cochrane Database Syst Rev. 2018. PMID 30480773 · DOI · PMC6516961
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-11-04; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-11-04.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.