Evidence map›Paper›PMID 24503248›Full record

ReviewJournal of reproductive immunology2014

Therapeutic potential of statins and the induction of heme oxygenase-1 in preeclampsia.

Wenda Ramma, Asif Ahmed

Registry-linked trialOpen access · hybridAbstract readReview
In one paragraph

Review in Journal of reproductive immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03648970 (Pravastatin to Prevent Preeclampsia and Reduce Maternal-Neonatal Mortality and Morbidity in High Risk Preeclampsia Patients), which is not on this map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
10.1field-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.

NCT03648970 phase2unknown statusnot on this mapstarted 2018, after this paper: background citation

Pravastatin to Prevent Preeclampsia and Reduce Maternal-Neonatal Mortality and Morbidity in High Risk Preeclampsia Patients

TypeinterventionalSponsorUniversitas AirlanggaRan2018 to 2020Enrolled280ConditionsPre-EclampsiaArmsPravastatin
3 · Its place in the literature

Who cites it

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 87 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Review
  6. Secondary prevention of preeclampsia.Frontiers in cell and developmental biology · 2025
    Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Dyslipidemia and the role of adipose tissue in early pregnancy in the BPH/5 mouse model for preeclampsia.American journal of physiology. Regulatory, integrative and comparative physiology · 2019
    Article
  15. Review
  16. Review
  17. Angiogenic factors: potential to change clinical practice in pre-eclampsia?BJOG : an international journal of obstetrics and gynaecology · 2018
    Review
  18. Review
  19. Article
  20. Observational
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

2 authors at 2 institutions in 2 countries.

Wenda RammaDepartment of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA. Electronic address: wendaramma0405@gmail.com.
Asif AhmedVascular Biology Laboratory, School of Medical Sciences, Aston University, Birmingham B4 7ET, England, United Kingdom.
Aston University · GBBeth Israel Deaconess Medical Center · US

Funding

Medical Research Council
6 · The paper itself

Abstract

Heme oxygenase (Hmox) is an endogenous system that offers protection against placental cytotoxic damage associated with preeclampsia. The Hmox1/carbon monoxide (CO) pathway inhibits soluble Flt-1 (sFlt-1) and soluble Endoglin (sEng). More importantly, statins induce Hmox1 and suppress the release of sFlt-1 and sEng; thus, statins and Hmox1 activators are potential novel therapeutic agents for treating preeclampsia. The contribution of the Hmox system to the pathogenesis of preeclampsia has been further indicated by the incidence of preeclampsia being reduced by a third in smokers, who had reduced levels of circulating sFlt-1. Interestingly, preeclamptic women exhale less CO compared with women with healthy pregnancies. Hmox1 is reduced prior to the increase in sFlt-1 as Hmox1 mRNA expression in the trophoblast is decreased in the first trimester in women who go on to develop preeclampsia. Induction of Hmox1 or exposure to CO or bilirubin has been shown to inhibit the release of sFlt-1 and sEng in animal models of preeclampsia. The functional benefit of statins and Hmox1 induction in women with preeclampsia is valid not only because they inhibit sFlt-1 release, but also because statins and Hmox1 are associated with anti-apoptotic, anti-inflammatory, and anti-oxidant properties. The StAmP trial is the first randomized control trial (RCT) evaluating the use of pravastatin to ameliorate severe preeclampsia. This proof-of-concept study will pave the way for future global RCT, the success of which will greatly contribute to achieving the United Nations Millennium Development Goals (MDG4 and MDG5) and offering an affordable and easily accessible therapy for preeclampsia.

Indexed as

AnimalsDisease Models, AnimalFemaleHeme Oxygenase-1HumansHydroxymethylglutaryl-CoA Reductase InhibitorsPre-EclampsiaPregnancyRandomized Controlled Trials as TopicUp-RegulationVascular Endothelial Growth Factor Receptor-1FLT1 protein, humanHeme Oxygenase-1HMOX1 protein, humanHydroxymethylglutaryl-CoA Reductase InhibitorsVascular Endothelial Growth Factor Receptor-1Carbon monoxide (CO)Heme oxygenase-1 (Hmox1)PreeclampsiaSoluble Endoglin (sEng)Soluble Flt-1 (sFlt-1)StatinsVascular endothelial growth factor (VEGF)

Identifiers

PMID24503248
PMCPMC4003533
OpenAlexW2126688155

What OpenQuestion holds

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LicenceCC BY
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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.