Evidence map›Paper›PMID 30503138›Full record

ArticleFertility and sterility2018

Simvastatin, at clinically relevant concentrations, affects human uterine leiomyoma growth and extracellular matrix production.

Minnie Malik, Joy Britten, Mostafa Borahay, James Segars, William H Catherino

Abstract read
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In one paragraph

Article in Fertility and sterility, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

27 citing papers in PubMed, 44 citations in OpenAlex.

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  10. The Role of Nanomedicine in Benign Gynecologic Disorders.Molecules (Basel, Switzerland) · 2024
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  14. Simvastatin-loaded liposome nanoparticles treatment for uterine leiomyoma in a patient-derived xenograft mouse model: a pilot study.Journal of obstetrics and gynaecology : the journal of the Institute of Obstetrics and Gynaecology · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 1 country.

Minnie MalikDepartment of Obstetrics and Gynecology, Uniformed Services University of the Health Sciences, Bethesda, Maryland.
Joy BrittenDepartment of Obstetrics and Gynecology, Uniformed Services University of the Health Sciences, Bethesda, Maryland.
Mostafa BorahayDivision of Reproductive Sciences and Women's Health Research, Department of Gynecology and Obstetrics, Johns Hopkins Medicine, Baltimore, Maryland.
James SegarsDivision of Reproductive Sciences and Women's Health Research, Department of Gynecology and Obstetrics, Johns Hopkins Medicine, Baltimore, Maryland.
William H CatherinoDepartment of Obstetrics and Gynecology, Uniformed Services University of the Health Sciences, Bethesda, Maryland. Electronic address: william.catherino@usuhs.edu.
Uniformed Services University of the Health Sciences · USJohns Hopkins Medicine · USJohns Hopkins University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo observe the antifibroid effects of therapeutic concentrations of simvastatin, which interferes with cholesterol biosynthesis, a known precursor of five major classes of steroid hormones, including progesterone and estrogen, which play a major role in the development and growth of uterine leiomyomas.

designTwo-dimensional and three-dimensional cell culture study of immortalized human leiomyoma and patient-matched myometrium cells treated with simvastatin.

settingUniversity laboratory. PATIENT(S): None. INTERVENTIONS(S): None. MAIN OUTCOME MEASURE(S): Cell proliferation, alteration in apoptotic signaling pathways, and extracellular matrix (ECM) protein production. RESULT(S): Simvastatin demonstrated a concentration-dependent antiproliferative effect on both the leiomyoma cells and the patient-matched myometrium cells, but a higher inhibitory effect at lower concentrations of simvastatin was observed in leiomyoma cells. Simvastatin also regulated leiomyoma cell apoptosis through a concentration-dependent increase in activity of caspase-3. Simvastatin significantly inhibited expression of major ECM proteins collagen I, collagen III, fibronectin, versican, and brevican in leiomyoma cells at concentrations as low as 10 CONCLUSION(S): Simvastatin induces apoptosis in uterine leiomyoma cells at low concentrations, as evidenced by increased active caspase levels. Furthermore, inhibited production of the ECM proteins may lead to reduction in tumor size. Simvastatin may represent a novel therapeutic treatment strategy for uterine leiomyomas.

Indexed as

ApoptosisCell ProliferationCollagenDose-Response Relationship, DrugExtracellular MatrixFemaleGlycoproteinsHumansLeiomyomaMyometriumSignal TransductionSimvastatinTumor Cells, CulturedUterine NeoplasmsVersicansCollagenGlycoproteinsSimvastatinVersicansapoptosiscollagensglycoproteinsLeiomyomamyometriumsimvastatinversican

Identifiers

PMID30503138
OpenAlexW2902858715

What OpenQuestion holds

Textmetadata
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.