ArticleFrontiers in cardiovascular medicine2015
Four Pathways Involving Innate Immunity in the Pathogenesis of Preeclampsia.
Article in Frontiers in cardiovascular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 2 of them syntheses that pooled it.
What it found
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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.
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.
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Who cites it
12 citing papers in PubMed, 2 syntheses or guidelines pooled it, 29 citations in OpenAlex.
- Association between maternal depressive symptoms during pregnancy and the risk of preeclampsia: a meta-analysis.Frontiers in psychiatry · 2026Pooled it
- 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 · 2021Pooled it
- Preeclamptic Placental CD19+ B Cells Are Causal to Hypertension During Pregnancy.Hypertension (Dallas, Tex. : 1979) · 2025Article
- Trained innate immunity as a potential link between preeclampsia and future cardiovascular disease.Frontiers in endocrinology · 2024Review
- Circulating miRNAs as Epigenetic Mediators of Periodontitis and Preeclampsia Association.Disease markers · 2022Article
- Placental Microbial Colonization and Its Association With Pre-eclampsia.Frontiers in cellular and infection microbiology · 2020Review
- Targeting toll-like receptor 4 signalling pathways: can therapeutics pay the toll for hypertension?British journal of pharmacology · 2019Review
- Exploration of the regulation and control mechanisms of miR-145 in trophoblast cell proliferation and invasion.Experimental and therapeutic medicine · 2018Article
- Immunological Tolerance, Pregnancy, and Preeclampsia: The Roles of Semen Microbes and the Father.Frontiers in medicine · 2017Article
- MicroRNAs: New Players in the Pathobiology of Preeclampsia.Frontiers in cardiovascular medicine · 2017Review
- Sphingolipids as a new factor in the pathomechanism of preeclampsia - Mass spectrometry analysis.PloS one · 2017Article
- Preeclampsia and health risks later in life: an immunological link.Seminars in immunopathology · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The maternal innate immune system plays an important role both in normal pregnancy as well as hypertensive disorders of pregnancy including preeclampsia (PE). We propose four pathways that involve excessive innate immunity that lead to most forms of PE. Pre-existing endothelial dysfunction plus pregnancy leads to an excessive innate immune response resulting in widespread inflammation, placental and renal dysfunction, vasoconstriction, and PE. Placental dysfunction due to shallow trophoblast invasion, inadequate spiral artery remodeling, and/or low placental perfusion initiates an innate immune response leading to excessive inflammation, endothelial and renal dysfunction, and PE. A heightened innate immune system due to pre-existing or acquired infections plus the presence of a paternally derived placenta and semi-allogeneic fetus cause an excessive innate immune response which manifests as PE. Lastly, an abnormal and excessive maternal immune response to pregnancy leads to widespread inflammation, organ dysfunction, and PE. We discuss the potential role of innate immunity in each of these scenarios, as well as the overlap, and how targeting the innate immune system might lead to therapies for the treatment of PE.
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Registered trials
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.