Evidence map›Paper›PMID 32337535›Full record

ReviewClinical science (London, England : 1979)2020

From animal models to patients: the role of placental microRNAs, miR-210, miR-126, and miR-148a/152 in preeclampsia.

Sonya Frazier, Martin W McBride, Helen Mulvana, Delyth Graham

Open access · hybridAbstract readReview
In one paragraph

Review in Clinical science (London, England : 1979), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.6field-weighted citation impact, top 5% 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

34 citing papers in PubMed, 58 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. MiR-26a-5p/EZH2 Mediates Wnt2 Promoter Methylation to Regulate Trophoblast Dysfunction.Combinatorial chemistry & high throughput screening · 2026
    Article
  5. Review
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  8. Screening and analysis of plasma differential lncRNA/mRNA in early pregnancy of preeclampsia.Malawi medical journal : the journal of Medical Association of Malawi · 2025
    Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
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  17. Review
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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

4 authors at 2 institutions in 1 country.

Sonya FrazierInstitute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, U.K.
Martin W McBrideInstitute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, U.K.
Helen MulvanaBiomedical Engineering, University of Strathclyde, Glasgow, U.K.
Delyth GrahamInstitute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, U.K.
University of Glasgow · GBUniversity of Strathclyde · GB

Funding

British Heart Foundation RE/13/5/30177
6 · The paper itself

Abstract

Placental microRNAs (miRNAs) regulate the placental transcriptome and play a pathological role in preeclampsia (PE), a hypertensive disorder of pregnancy. Three PE rodent model studies explored the role of placental miRNAs, miR-210, miR-126, and miR-148/152 respectively, by examining expression of the miRNAs, their inducers, and potential gene targets. This review evaluates the role of miR-210, miR-126, and miR-148/152 in PE by comparing findings from the three rodent model studies with in vitro studies, other animal models, and preeclamptic patients to provide comprehensive insight into genetic components and pathological processes in the placenta contributing to PE. The majority of studies demonstrate miR-210 is upregulated in PE in part driven by HIF-1α and NF-κBp50, stimulated by hypoxia and/or immune-mediated processes. Elevated miR-210 may contribute to PE via inhibiting anti-inflammatory Th2-cytokines. Studies report an up- and downregulation of miR-126, arguably reflecting differences in expression between cell types and its multifunctional capacity. MiR-126 may play a pro-angiogenic role by mediating the PI3K-Akt pathway. Most studies report miR-148/152 family members are upregulated in PE. Evidence suggests they may inhibit DNA methylation of genes involved in metabolic and inflammatory pathways. Given the genetic heterogeneity of PE, it is unlikely that a single placental miRNA is a suitable therapeutic target for all patients. Investigating miRNAs in PE subtypes in patients and animal models may represent a more appropriate approach going forward. Developing methods for targeting placental miRNAs and specific placental cell types remains crucial for research seeking to target placental miRNAs as a novel treatment for PE.

Indexed as

AnimalsDisease Models, AnimalFemaleHumansMicroRNAsPlacentaPre-EclampsiaPregnancyMicroRNAsMIRN126 microRNA, humanMIRN148 microRNA, humanMIRN152 microRNA, humanMIRN210 microRNA, humanmicroRNAplacentapreeclampsiapregnancy

Identifiers

PMID32337535
PMCPMC7239341
OpenAlexW3019463509

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.