Evidence map›Paper›PMID 33013837›Full record

ReviewFrontiers in immunology2020

Mechanisms of Key Innate Immune Cells in Early- and Late-Onset Preeclampsia.

Ingrid Aneman, Dillan Pienaar, Sonja Suvakov, Tatjana P Simic, Vesna D Garovic, Lana McClements

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
133citing papers in PubMed, 5 pooled it
10.8field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

133 citing papers in PubMed, 5 syntheses or guidelines pooled it, 223 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Association Between TLR4 Gene Polymorphisms and Risk of Preeclampsia: Systematic Review and Meta-Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2021
    Pooled it
  5. Pooled it
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Subtype specific immune-metabolic reprogramming in preeclampsia revealed by multiomics and serum biomarkers.Hypertension research : official journal of the Japanese Society of Hypertension · 2026
    Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Current Understanding on Hypertensive Disorders in Pregnancy.International journal of general medicine · 2026
    Review
  19. PeerJ · 2026
    Article
  20. Article

73 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 3 countries.

Ingrid AnemanFaculty of Science, School of Life Sciences, University of Technology Sydney, Sydney, NSW, Australia.
Dillan PienaarFaculty of Science, School of Life Sciences, University of Technology Sydney, Sydney, NSW, Australia.
Sonja SuvakovDivision of Nephrology and Hypertension, Department of Internal Medicine, Mayo Clinic, Rochester, MN, United States.
Tatjana P SimicFaculty of Medicine, Institute of Medical and Clinical Biochemistry, University of Belgrade, Belgrade, Serbia.
Vesna D GarovicDivision of Nephrology and Hypertension, Department of Internal Medicine, Mayo Clinic, Rochester, MN, United States.
Lana McClementsFaculty of Science, School of Life Sciences, University of Technology Sydney, Sydney, NSW, Australia.
University of Technology Sydney · AUWinnMed · USUniversity of Belgrade · RS

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Preeclampsia is a complex cardiovascular disorder of pregnancy with underlying multifactorial pathogeneses; however, its etiology is not fully understood. It is characterized by the new onset of maternal hypertension after 20 weeks of gestation, accompanied by proteinuria, maternal organ damage, and/or uteroplacental dysfunction. Preeclampsia can be subdivided into early- and late-onset phenotypes (EOPE and LOPE), diagnosed before 34 weeks or from 34 weeks of gestation, respectively. Impaired placental development in early pregnancy and subsequent growth restriction is often associated with EOPE, while LOPE is associated with maternal endothelial dysfunction. The innate immune system plays an essential role in normal progression of physiological pregnancy and fetal development. However, inappropriate or excessive activation of this system can lead to placental dysfunction or poor maternal vascular adaptation and contribute to the development of preeclampsia. This review aims to comprehensively outline the mechanisms of key innate immune cells including macrophages, neutrophils, natural killer (NK) cells, and innate B1 cells, in normal physiological pregnancy, EOPE and LOPE. The roles of the complement system, syncytiotrophoblast extracellular vesicles and mesenchymal stem cells (MSCs) are also discussed in the context of innate immune system regulation and preeclampsia. The outlined molecular mechanisms, which represent potential therapeutic targets, and associated emerging treatments, are evaluated as treatments for preeclampsia. Therefore, by addressing the current understanding of innate immunity in the pathogenesis of EOPE and LOPE, this review will contribute to the body of research that could lead to the development of better diagnosis, prevention, and treatment strategies. Importantly, it will delineate the differences in the mechanisms of the innate immune system in two different types of preeclampsia, which is necessary for a more personalized approach to the monitoring and treatment of affected women.

Indexed as

FemaleGestational AgeHumansImmunity, InnatePre-EclampsiaPregnancyTime Factorsearly-onset preeclampsiaimmune cellsinflammationinnate immunitylate-onset preeclampsiapreeclampsiapregnancy

Identifiers

PMID33013837
PMCPMC7462000
OpenAlexW3063846960

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.