Evidence map›Paper›PMID 38825645›Full record

ArticleExperimental & molecular medicine2024

Alleviation of preeclampsia-like symptoms through PlGF and eNOS regulation by hypoxia- and NF-κB-responsive miR-214-3p deletion.

Suji Kim, Sungbo Shim, Jisoo Kwon, Sungwoo Ryoo, Junyoung Byeon, Jungwoo Hong, Jeong-Hyung Lee, Young-Guen Kwon, Ji-Yoon Kim, Young-Myeong Kim

Erratum issuedAbstract read
In one paragraph

Article in Experimental & molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
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

17 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Deletion of endothelial KLF4 as a model for preeclampsia.bioRxiv : the preprint server for biology · 2026
    Article
  6. Review
  7. Review
  8. Article
  9. Trophoblast adaptation to hypoxia: balance and dysfunction.Cell communication and signaling : CCS · 2025
    Review
  10. Article
  11. Review
  12. NFĸB and its inhibitors in preeclampsia: mechanisms and potential interventions.Naunyn-Schmiedeberg's archives of pharmacology · 2025
    Review
  13. Article
  14. Article
  15. Article
  16. Vitamin DExperimental biology and medicine (Maywood, N.J.) · 2025
    Article
  17. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors.

Suji KimDepartment of Molecular and Cellular Biochemistry, School of Medicine, Kangwon National University, Chuncheon, 24341, Republic of Korea.
Sungbo ShimDepartment of Biochemistry, Chungbuk National University, Cheongju, 28644, Republic of Korea.
Jisoo KwonDepartment of Anesthesiology and Pain Medicine, Hanyang University Hospital, Hanyang University College of Medicine, Seoul, 04763, Republic of Korea.
Sungwoo RyooDepartment of Biological Sciences, Kangwon National University, Chuncheon, 24341, Republic of Korea.
Junyoung ByeonDepartment of Biochemistry, College of Natural Sciences, Kangwon National University, Chuncheon, 24341, Republic of Korea.
Jungwoo HongDepartment of Biochemistry, College of Natural Sciences, Kangwon National University, Chuncheon, 24341, Republic of Korea.
Jeong-Hyung LeeDepartment of Biochemistry, College of Natural Sciences, Kangwon National University, Chuncheon, 24341, Republic of Korea.
Young-Guen KwonAdvanced Institute of Technology, Curacle Co. Ltd, Seoul, 06694, Republic of Korea.
Ji-Yoon KimDepartment of Anesthesiology and Pain Medicine, Hanyang University Hospital, Hanyang University College of Medicine, Seoul, 04763, Republic of Korea. irisjyoo@hanyang.ac.kr.
Young-Myeong KimDepartment of Molecular and Cellular Biochemistry, School of Medicine, Kangwon National University, Chuncheon, 24341, Republic of Korea. ymkim@kangwon.ac.kr.ORCID http://orcid.org/0000-0002-8326-7768

Funding

National Research Foundation of Korea (NRF) 2022R1A2C3005747
6 · The paper itself

Abstract

Preeclampsia is caused by placental hypoxia and systemic inflammation and is associated with reduced placental growth factor (PlGF) and endothelial nitric oxide synthase (eNOS) levels. The molecular signaling axes involved in this process may play a role in the pathogenesis of preeclampsia. Here, we found that hypoxic exposure increased hypoxia-inducible factor-1α (HIF-1α)/Twist1-mediated miR-214-3p biogenesis in trophoblasts, suppressing PlGF production and trophoblast invasion. TNF-α stimulation increased NF-κB-dependent miR-214-3p expression in endothelial cells, impairing eNOS expression and causing endothelial dysfunction. Synthetic miR-214-3p administration to pregnant mice decreased PlGF and eNOS expression, resulting in preeclampsia-like symptoms, including hypertension, proteinuria, and fetal growth restriction. Conversely, miR-214-3p deletion maintained the PlGF and eNOS levels in hypoxic pregnant mice, alleviating preeclampsia-like symptoms and signs. These findings provide new insights into the role of HIF-1/Twist1- and NF-κB-responsive miR-214-3p-dependent PlGF and eNOS downregulation in the pathogenesis of preeclampsia and establish miR-214-3p as a therapeutic or preventive target for preeclampsia and its complications.

Indexed as

MicroRNAsNF-kappa BNitric Oxide Synthase Type IIIPlacenta Growth FactorPre-EclampsiaAnimalsDisease Models, AnimalFemaleGene Expression RegulationHumansHypoxiaHypoxia-Inducible Factor 1, alpha SubunitMicePregnancyTrophoblastsHypoxia-Inducible Factor 1, alpha SubunitMicroRNAsMirn214 microRNA, mouseNF-kappa BNitric Oxide Synthase Type IIIPlacenta Growth Factor

Identifiers

PMID38825645
PMCPMC11263402

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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.