Evidence map›Paper›PMID 42173876›Full record

ArticleNPJ biofilms and microbiomes2026

Parabacteroides goldsteinii and its metabolite 7-KLCA attenuate endometriosis via TGR5 to reprogram macrophages by modulating the PPARγ/GPR132 axis.

Yun Chen, Yuqing Qiu, Feifei Pan, Yanqin Zheng, Jingyao Wang, Kunxiang Gong, Lirong Guo, Yiming Song, Zixin Tao, Kun Shi

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PubMed Full text at PMC Publisher
In one paragraph

Article in NPJ biofilms and microbiomes, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

10 authors.

Yun ChenDepartment of Gynecology and Obstetrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.
Yuqing QiuDepartment of Gynecology and Obstetrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.
Feifei PanDepartment of Gynecology and Obstetrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.
Yanqin ZhengDepartment of Gynecology and Obstetrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.
Jingyao WangDepartment of Gynecology and Obstetrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.
Kunxiang GongDepartment of Gynecology and Obstetrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.
Lirong GuoDepartment of Gynecology and Obstetrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.
Yiming SongDepartment of Gynecology and Obstetrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.
Zixin TaoDepartment of Gynecology and Obstetrics, Guangzhou First People's Hospital, South China University of Technology, Guangzhou, China. 329011915@qq.com.
Kun ShiDepartment of Gynecology and Obstetrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China. shikun28@hotmail.com.

Funding

Basic and Applied Basic Research Foundation of Guangdong Province 2022A1515220127China Postdoctoral Science Foundation 2024M750643Guangzhou Health Science and Technology Youth Talent Cultivation Project 20261A031007National Natural Science Foundation of China 82072859
6 · The paper itself

Abstract

Endometriosis (EMS) remains understudied in effective management strategies. The interplay between macrophage dysfunction and microbiota-derived immune signals emerges as a potential mechanism in EMS pathogenesis, suggesting its relevance for future therapeutic exploration. In this study, we established mouse models to demonstrate that gut microbiota modulated EMS development. Integrated microbial and metabolomic profiling identified Parabacteroides goldsteinii (Pg) as a promising probiotic candidate, whose downstream metabolite 7-ketolithocholic acid (7-KLCA) exhibiting therapeutic efficacy in ameliorating EMS phenotypes upon supplementation. Mechanistically, Pg reshapes its bile acid (BA) metabolism to elevate 7-KLCA. This bioactive metabolite acts via the receptor TGR5 to suppress PPARγ expression and activate GPR132, thereby enhancing efferocytosis and promoting M1 macrophage polarization. These findings uncover a gut-metabolite-immune regulatory axis through which Pg reprograms macrophage function to restrain EMS progression, offering a potential microbial perspective for this chronic condition.

Indexed as

EndometriosisLithocholic AcidMacrophagesPPAR gammaProbioticsReceptors, G-Protein-CoupledAnimalsDisease Models, AnimalEfferocytosisFemaleHumansMiceGpbar1 protein, mouseLithocholic AcidPPAR gammaReceptors, G-Protein-Coupled

Identifiers

PMID42173876
PMCPMC13473097

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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.