Evidence map›Paper›PMID 33693775›Full record

ArticleMolecular human reproduction2021

Tofacitinib alters STAT3 signaling and leads to endometriosis lesion regression.

Alexander M Kotlyar, Ramanaiah Mamillapalli, Valerie A Flores, Hugh S Taylor

Open access · bronzeAbstract read
In one paragraph

Article in Molecular human reproduction, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

28 citing papers in PubMed, 42 citations in OpenAlex.

  1. L-ICON3 Suppresses Endometriosis in a Murine Model.Journal of molecular medicine (Berlin, Germany) · 2026
    Article
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  9. The interplay between endometriosis and obesity.Trends in endocrinology and metabolism: TEM · 2025
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Is JAK Inhibitor A Therapeutic Option For Endometriosis?Journal of obstetrics and gynaecology of India · 2025
    Article
  15. Nanoceria as a non-steroidal anti-inflammatory drug for endometriosis theranostics.Journal of controlled release : official journal of the Controlled Release Society · 2025
    Article
  16. Article
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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

4 authors at 1 institution in 1 country.

Alexander M KotlyarDepartment of Obstetrics, Gynecology, and Reproductive Sciences, Yale School of Medicine, Yale University, New Haven, CT, USA.
Ramanaiah MamillapalliDepartment of Obstetrics, Gynecology, and Reproductive Sciences, Yale School of Medicine, Yale University, New Haven, CT, USA.
Valerie A FloresDepartment of Obstetrics, Gynecology, and Reproductive Sciences, Yale School of Medicine, Yale University, New Haven, CT, USA.
Hugh S TaylorDepartment of Obstetrics, Gynecology, and Reproductive Sciences, Yale School of Medicine, Yale University, New Haven, CT, USA.
Yale University · US

Funding

Pre-IVF treatment with a GnRH antagonist in women with endometriosis - A prospective double blind placebo controlled trial (Pregnant) - Application 1/4R01HD100336 · NICHD · YALE UNIVERSITY · PI TAYLOR, HUGH SMITH, ZHANG, HEPING · 2019 to 2023
$5.5M
NICHD NIH HHS R01 HD100336
6 · The paper itself

Abstract

Endometriosis is a widespread gynecologic condition affecting up to 15% of women of reproductive age. The Janus kinase/signal transducer and activator of transcription (JAK/STAT3) pathway is upregulated in endometriosis and is a therapeutic target. Here we sought to determine the effect of Tofacitinib, a JAK inhibitor in widespread clinical use, on JAK/STAT signaling in endometriosis and lesion growth. Endometriosis was surgically induced in C57BL/6 mice using homologous uterine horn transplantation. Lesions were allowed to form over 4 weeks followed by Tofacitinib (10 mg/kg) or vehicle administered by oral gavage over 4 weeks. Tofacitinib treatment in vivo led to endometriosis lesion regression and reduced adhesion burden compared to vehicle treatment. In vitro studies on Ishikawa cells showed that Tofacitinib reduced hypoxia-inducible factor 1α and vascular endothelial growth factor mRNA levels at 12 and 24 h. Western blot analysis showed that Tofacitinib effectively reduced STAT3 phosphorylation in Ishikawa cells and human primary stromal and epithelial cells from eutopic endometrium of patients with and without endometriosis. This study suggests that the inhibition of JAK/STAT signaling using Tofacitinib may be a viable method for the treatment of endometriosis.

Indexed as

EndometriosisAnimalsFemaleHumansMiceMice, Inbred C57BLPiperidinesPyrimidinesSTAT3 Transcription FactorVascular Endothelial Growth Factor APiperidinesPyrimidinesSTAT3 protein, humanSTAT3 Transcription FactortofacitinibVascular Endothelial Growth Factor Aendometriosisendometriumhypoxia-inducible factor 1αJAK/STATSTAT3 phosphorylationTofacitinibvascular endothelial growth factor

Identifiers

PMID33693775
PMCPMC8454207
OpenAlexW3133957550

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.