Targeting TLR4 Attenuates Endometriosis Progression by Suppressing NF-κB/NLRP3 Inflammasome Activation and Angiogenesis.

Yunlei Cao, Xiangxiang Zhu, Xinxin Hou, Ding Ding

Abstract read

In one paragraph

Article in International journal of molecular sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it

0cells of the map it votes in

1citing papers in PubMed

–field-weighted citation impact

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

1 citing paper in PubMed.

The microbiome-inflammasome axis in endometriosis-associated chronic pelvic pain: mechanisms and therapeutic opportunities from an immunological perspective.Frontiers in immunology · 2026
Review

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.

Yunlei CaoDepartment of General Gynecology, Obstetrics & Gynecology Hospital of Fudan University, Shanghai Key Lab of Reproduction and Development, Shanghai Key Lab of Female Reproductive Endocrine Related Diseases, Shanghai 200433, China.

Xiangxiang ZhuSchool of Integrative Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China.

Xinxin HouSchool of Integrative Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China.

Ding DingDepartment of General Gynecology, Obstetrics & Gynecology Hospital of Fudan University, Shanghai Key Lab of Reproduction and Development, Shanghai Key Lab of Female Reproductive Endocrine Related Diseases, Shanghai 200433, China.

Funding

National Natural Science Foundation of China 82571900 to DD

6 · The paper itself

Abstract

Endometriosis is a chronic inflammatory disorder affecting approximately 10% of reproductive-age women, yet non-hormonal therapeutic options remain limited. This study investigates the role of the TLR4/NF-κB/NLRP3 inflammasome axis in endometriosis pathogenesis and evaluates the therapeutic potential of pharmacologic TLR4 inhibition. Ectopic endometriotic tissues, eutopic endometrium, and peritoneal fluid were collected from 15 patients with ovarian endometriosis and 15 control subjects. The endometriotic epithelial cell line 11Z was stimulated with LPS and ATP with or without the TLR4 inhibitor TAK-242. A murine endometriosis model was established in wild-type C57BL/6 and TLR4

Indexed as

EndometriosisInflammasomesNeovascularization, PathologicNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinToll-Like Receptor 4AdultAnimalsCell LineDisease Models, AnimalDisease ProgressionEndometriumFemaleHumansMiceMice, Inbred C57BLethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-ene-1-carboxylateInflammasomesNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinSulfonamidesTLR4 protein, humanTlr4 protein, mouseToll-Like Receptor 4angiogenesisendometriosisIL-1βNLRP3 inflammasomeTAK-242toll-like receptor 4

Identifiers

PMID42123727

DOI10.3390/ijms27094151

PMCPMC13164178

What OpenQuestion holds

Textmetadata

LicenceCC BY

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Registered trials

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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.