Evidence mapPaperPMID 35351413Full record

ArticleAmerican journal of obstetrics and gynecology2022

Endometriosis promotes atherosclerosis in a murine model.

Ramanaiah Mamillapalli, Nikoletta Toffoloni, Shutaro Habata, Huang Qunhua, Rula Atwani, Nina Stachenfeld, Hugh S Taylor

Open access · greenAbstract read
In one paragraph

Article in American journal of obstetrics and gynecology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 2 pooled it
2.6field-weighted citation impact, top 11% 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

7 citing papers in PubMed, 2 syntheses or guidelines pooled it, 15 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Article
  6. Physical Activity in Women with Endometriosis: Less or More Compared with a Healthy Control?International journal of environmental research and public health · 2023
    Article
  7. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Ramanaiah MamillapalliDepartment of Obstetrics, Gynecology, and Reproductive Sciences, Yale School of Medicine, New Haven, CT. Electronic address: ramana.mamillapalli@gmail.com.
Nikoletta ToffoloniDepartment of Obstetrics, Gynecology, and Reproductive Sciences, Yale School of Medicine, New Haven, CT.
Shutaro HabataDepartment of Obstetrics, Gynecology, and Reproductive Sciences, Yale School of Medicine, New Haven, CT.
Huang QunhuaDepartment of Surgery (Cardiac Surgery), Yale School of Medicine, New Haven, CT.
Rula AtwaniDepartment of Obstetrics, Gynecology, and Reproductive Sciences, Yale School of Medicine, New Haven, CT.
Nina StachenfeldDepartment of Obstetrics, Gynecology, and Reproductive Sciences, Yale School of Medicine, New Haven, CT.
Hugh S TaylorDepartment of Obstetrics, Gynecology, and Reproductive Sciences, Yale School of Medicine, New Haven, CT. Electronic address: hugh.taylor@yale.edu.
Yale University · US

Funding

Yale Clinical and Translational Science AwardUL1TR001863 · YALE UNIVERSITY · 2025 to 2025
$9.9M
NCATS NIH HHS UL1 TR001863NICHD NIH HHS R01 HD076422NICHD NIH HHS U54 HD052668
6 · The paper itself

Abstract

backgroundEpidemiologic studies have demonstrated an association between endometriosis and the subsequent development of cardiovascular disease. The direct effect of endometriosis on the progression of atherosclerotic, if any, has not been previously characterized. Endometriosis leads to systemic inflammation that could have consequences for cardiovascular health. Here, we reported the effects of endometriosis on the development of atherosclerosis in a murine model.

objectiveThis study aimed to determine the contribution of endometriosis in promoting cardiovascular disease in a murine model of endometriosis. STUDY

designEndometriosis was induced in 18 apolipoprotein E-null mice, the standard murine model used to study atherosclerosis. Mice of the same strain were used as controls (n=18) and underwent sham surgery without inducing endometriosis. The formation of endometriotic lesions was confirmed after 25 weeks of induction. Atherosclerotic lesions were subjected to hematoxylin and eosin staining followed by measurement of the aortic root luminal area and wall thickness. The whole aorta was isolated, and Oil Red O staining was performed to quantify the lipid deposits or plaque formation; moreover, biochemical assays were carried out in serum to determine the levels of lipids and inflammatory-related cytokines.

resultsApolipoprotein E mice with endometriosis exhibited increased aortic atherosclerosis compared with controls as measured using Oil Red O staining (7.9% vs 3.1%, respectively; P=.0004). Mice with endometriosis showed a significant 50% decrease in the aortic luminal area compared with sham mice (0.85 mm

conclusionOur study used a murine model to determine the effect of endometriosis on atherosclerosis. Inflammation-related cytokines interleukin 1 alpha, interleukin 6, interferon gamma, and vascular endothelial growth factor (angiogenic factor) released by endometriotic lesions may contribute to the increased cardiovascular risks in women with endometriosis. To reduce the risk of cardiovascular disease, early identification and treatment of endometriosis are essential. Future treatments targeting inflammatory cytokines may help reduce the long-term risk of cardiovascular disease in women with endometriosis.

Indexed as

AtherosclerosisCardiovascular DiseasesEndometriosisPlaque, AtheroscleroticAnimalsDisease Models, AnimalFemaleHumansInflammationInterferon-gammaInterleukin-1alphaInterleukin-6MiceMice, Inbred C57BLMice, KnockoutVascular Endothelial Growth Factor AInterferon-gammaInterleukin-1alphaInterleukin-6Vascular Endothelial Growth Factor Aapolipoprotein E miceatherosclerosiscardiovascular diseasecytokinesendometriosisinflammationplaques

Identifiers

PMID35351413
PMCPMC9308711
OpenAlexW4221074333

What Socratic holds

Textmetadata
LicenceTDM
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.