Evidence map›Paper›PMID 25739077›Full record

ReviewInternational journal of molecular sciences2015

Nitric oxide and reactive oxygen species in the pathogenesis of preeclampsia.

Keiichi Matsubara, Takashi Higaki, Yuko Matsubara, Akihiro Nawa

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed, 2 pooled it
16.2field-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

94 citing papers in PubMed, 2 syntheses or guidelines pooled it, 238 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Review
  5. Observational
  6. Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. The impact of neonicotinoid pesticides on reproductive health.Toxicological sciences : an official journal of the Society of Toxicology · 2025
    Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Secondary prevention of preeclampsia.Frontiers in cell and developmental biology · 2025
    Review
  17. Review
  18. Article
  19. Article
  20. Nitrogen Oxide (NO) in the Pathogenesis of Preeclampsia.Bulletin of experimental biology and medicine · 2024
    Article

34 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

4 authors at 1 institution in 1 country.

Keiichi MatsubaraDepartment of Obstetrics and Gynecology, Ehime University School of Medicine, Ehime 791-0295, Japan. keiichi@m.ehime-u.ac.jp.
Takashi HigakiDepartment of Pediatrics, Ehime University School of Medicine, Ehime 791-0295, Japan. higaki@m.ehime-u.ac.jp.
Yuko MatsubaraDepartment of Obstetrics and Gynecology, Ehime University School of Medicine, Ehime 791-0295, Japan. takeyu@m.ehime-u.ac.jp.
Akihiro NawaDepartment of Obstetrics and Gynecology, Ehime University School of Medicine, Ehime 791-0295, Japan. nawa2011@m.ehime-u.ac.jp.
Ehime University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Preeclampsia (PE) is characterized by disturbed extravillous trophoblast migration toward uterine spiral arteries leading to increased uteroplacental vascular resistance and by vascular dysfunction resulting in reduced systemic vasodilatory properties. Its pathogenesis is mediated by an altered bioavailability of nitric oxide (NO) and tissue damage caused by increased levels of reactive oxygen species (ROS). Furthermore, superoxide (O2-) rapidly inactivates NO and forms peroxynitrite (ONOO-). It is known that ONOO- accumulates in the placental tissues and injures the placental function in PE. In addition, ROS could stimulate platelet adhesion and aggregation leading to intravascular coagulopathy. ROS-induced coagulopathy causes placental infarction and impairs the uteroplacental blood flow in PE. The disorders could lead to the reduction of oxygen and nutrients required for normal fetal development resulting in fetal growth restriction. On the other hand, several antioxidants scavenge ROS and protect tissues against oxidative damage. Placental antioxidants including catalase, superoxide dismutase (SOD), and glutathione peroxidase (GPx) protect the vasculature from ROS and maintain the vascular function. However, placental ischemia in PE decreases the antioxidant activity resulting in further elevated oxidative stress, which leads to the appearance of the pathological conditions of PE including hypertension and proteinuria. Oxidative stress is defined as an imbalance between ROS and antioxidant activity. This review provides new insights about roles of oxidative stress in the pathophysiology of PE.

Indexed as

Oxidative StressAntioxidantsFemaleHumansModels, BiologicalNitric OxidePlacentaPre-EclampsiaPregnancyReactive Oxygen SpeciesAntioxidantsNitric OxideReactive Oxygen Species

Identifiers

PMID25739077
PMCPMC4394437
OpenAlexW1982391253

What Socratic 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 Socratic graph.