Evidence map›Paper›PMID 23539633›Full record

ReviewHuman reproduction update

Endometriosis: hormone regulation and clinical consequences of chemotaxis and apoptosis.

Fernando M Reis, Felice Petraglia, Robert N Taylor

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Human reproduction update. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
120citing papers in PubMed, 2 pooled it
20.6field-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

120 citing papers in PubMed, 2 syntheses or guidelines pooled it, 261 citations in OpenAlex.

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  5. Decreased PD-1Scandinavian journal of immunology · 2026
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60 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

3 authors at 3 institutions in 3 countries.

Fernando M ReisDepartment of Obstetrics and Gynecology, University of Minas Gerais, Belo Horizonte, Brazil.
Felice Petraglia
Robert N Taylor
Universidade Federal de Minas Gerais · BRUniversity of Siena · ITWake Forest University · US

Funding

Role of C/EBPb in Uterine Decidualization and ImplantationU54HD055787 · NICHD · UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN · PI BAGCHI, MILAN K · 2008 to 2012
$6.8M
1/2-Atlanta Center for Translational Research in Endometriosis (ACTRE)U01HD066439 · NICHD · EMORY UNIVERSITY · PI SIDELL, NEIL, THOMPSON, WINSTON E · 2010 to 2014
$1.4M
NICHD NIH HHS U01HD66439NICHD NIH HHS U54HD55787
6 · The paper itself

Abstract

backgroundThe recruitment of immune cells by chemokines and the regulation of endometrial cell apoptosis are critical aspects of endometriosis biology. Here, we review the local (paracrine) and systemic hormone (endocrine) modulation of these two specific, but highly related phenomena.

methodsWe searched Pubmed for items published in English between September 1991 and September 2011 and selected the studies evaluating the effects of hormones on chemokines or apoptosis in normal human endometrium and endometriosis.

resultsEstradiol has proinflammatory and antiapoptotic effects in endometrial cells, and these effects appear to be exacerbated in women with endometriosis. In these women, physiological estradiol concentrations are able to induce an enhanced inflammatory response mediated by local chemokine production and to reinforce mechanisms of cell survival mediated by extracellular signal-regulated kinases and Bcl-2. The main effect of progestogens is to inhibit interleukin-8 and other chemokines in stromal cells from both eutopic and ectopic endometrium. Progesterone is also effective in inducing apoptosis in endometrial and endometriotic cells through the inhibition of Bcl-2 and nuclear factor-κB.

conclusionsEstrogens and progestogens modulate chemotaxis and apoptosis in human endometrium and endometriotic cells and tissues. These endocrine and paracrine pathways are perturbed in women with endometriosis, contributing to inflammatory responses, abnormal tissue remodeling, therapeutic refractoriness and disease persistence. Ultimately, they promote adhesion formation and the clinical symptoms of pelvic pain and infertility. A more detailed understanding of the molecular mechanisms involved will offer new opportunities for novel pharmacological strategies to diagnose and treat endometriosis.

Indexed as

ApoptosisChemotaxisEndometriosisEndometriumEstrogensExtracellular Signal-Regulated MAP KinasesFemaleHumansInterleukin-8NF-kappa BProgestinsStromal CellsEstrogensExtracellular Signal-Regulated MAP KinasesInterleukin-8NF-kappa BProgestinsapoptosischemokinesendometriosisendometriumhormones

Identifiers

PMID23539633
PMCPMC3682670
OpenAlexW2145057288

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.