Evidence map›Paper›PMID 23598784›Full record

ReviewMinerva ginecologica2013

Medical management of endometriosis: emerging evidence linking inflammation to disease pathophysiology.

K L Bruner-Tran, J L Herington, A J Duleba, H S Taylor, K G Osteen

Open access · greenAbstract readReview
In one paragraph

Review in Minerva ginecologica, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
11.2field-weighted citation impact, top 2% 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

38 citing papers in PubMed, 60 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. The gut microbiota and endometriosis: From pathogenesis to diagnosis and treatment.Frontiers in cellular and infection microbiology · 2022
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Environmental Endocrine Disruptors and Endometriosis.Advances in anatomy, embryology, and cell biology · 2020
    Review
  15. Article
  16. Review
  17. Progesterone Receptor Status Predicts Response to Progestin Therapy in Endometriosis.The Journal of clinical endocrinology and metabolism · 2018
    Article
  18. Article
  19. Article
  20. Article
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

5 authors at 1 institution in 1 country.

K L Bruner-TranDepartment of Obstetrics and Gynecology, Vanderbilt University School of Medicine, Nashville, TN, USA.
J L Herington
A J Duleba
H S Taylor
K G Osteen
Vanderbilt University · US

Funding

Tissue Factor and EmdometriosisU54HD052668 · NICHD · YALE UNIVERSITY · PI TAYLOR, HUGH SMITH · 2007 to 2011
$6.6M
Dioxin Exposure and the Invasive Pathogenesis of EndometriosisR01ES014942 · NIEHS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BRUNER-TRAN, KAYLON L, OSTEEN, KEVIN G · 2006 to 2016
$3.5M
Loss of Complement-Protective CD55 Expression in EndometriosisR01HD055648 · NICHD · VANDERBILT UNIVERSITY · PI OSTEEN, KEVIN G · 2007 to 2011
$2.4M
Reproductive Biology: Training for the 21st CenturyT32HD007043 · NICHD · VANDERBILT UNIVERSITY · PI OSTEEN, KEVIN G · 1985 to 2011
$2.3M
NICHD NIH HHS R01 HD055648NICHD NIH HHS T32 HD007043NICHD NIH HHS U54 HD052668NIEHS NIH HHS R01 ES014942
6 · The paper itself

Abstract

Progesterone action normally mediates the balance between anti-inflammatory and proinflammatory processes throughout the female reproductive tract. However, in women with endometriosis, endometrial progesterone resistance, characterized by alterations in progesterone responsive gene and protein expression, is now considered a central element in disease pathophysiology. Recent studies additionally suggest that the peritoneal microenvironment of endometriosis patients exhibits altered physiological characteristics that may further promote inflammation-driven disease development and progression. Within this review, we summarize our current understanding of the pathogenesis of endometriosis with an emphasis on the role that inflammation plays in generating not only the progesterone-resistant eutopic endometrium but also a peritoneal microenvironment that may contribute significantly to disease establishment. Viewing endometriosis from the emerging perspective that a progesterone resistant endometrium and an immunologically compromised peritoneal microenvironment are biologically linked risk factors for disease development provides a novel mechanistic framework to identify new therapeutic targets for appropriate medical management.

Indexed as

AnimalsEndometriosisEndometriumFemaleForecastingGenital Diseases, FemaleGenotypeHumansInflammationProgesteroneProgesterone

Identifiers

PMID23598784
PMCPMC3718308
OpenAlexW1520611110

What OpenQuestion 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 OpenQuestion graph.