Evidence map›Paper›PMID 39680750›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

Clostridium Scindens Protects Against Vancomycin-Induced Cholestasis and Liver Fibrosis by Activating Intestinal FXR-FGF15/19 Signaling.

Jintao Xiao, Yanliang Hou, Xingyang Luo, Yuhao Zhu, Wenhu Li, Bingbing Li, LinXiang Zhou, Xia Chen, Ying Guo, Xiaomei Zhang and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

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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

12 authors.

Jintao XiaoDepartment of Gastroenterology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.ORCID https://orcid.org/0000-0002-4072-7816
Yanliang HouDepartment of Gastroenterology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.
Xingyang LuoDepartment of Gastroenterology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.
Yuhao ZhuDepartment of Gastroenterology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.
Wenhu LiDepartment of Gastroenterology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.
Bingbing LiDepartment of Gastroenterology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.
LinXiang ZhouDepartment of Gastroenterology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.
Xia ChenDepartment of Clinical Laboratory, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.
Ying GuoDepartment of Clinical Pharmacology, Xiangya Hospital, Hunan Key Laboratory of Pharmacogenetics, Central South University, Changsha, Hunan, 410008, China.
Xiaomei ZhangDepartment of Gastroenterology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.
Haiyue HeDepartment of Gastroenterology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.
Xiaowei LiuDepartment of Gastroenterology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.ORCID https://orcid.org/0000-0002-1193-4277

Funding

National Key Research and Development Program of China 2023YFC2506003National Natural Science Foundation of China 82170599National Natural Science Foundation of China 82230019National Natural Science Foundation of China 82341225
6 · The paper itself

Abstract

Primary sclerosing cholangitis (PSC) is characterized by abnormal bile acid metabolites and altered gut microbiota, with no effective treatments available. Vancomycin, a glycopeptide antibiotic, has emerged as a promising candidate. However, the mechanism by which vancomycin impacts the progression of PSC remains unknown. Mice treated with vancomycin exhibit increased hepatic collagen deposition and injury, due to the inhibition of intestinal FXR-FGF15/19 axis and the elevation of bile acid levels. These effects are associated with the reduction in Clostridia XIVa, especially Clostridium scindens (C. scindens). Gavage of C. scindens alleviates vancomycin-induced bile acid accumulation and liver fibrosis via activating intestinal FXR-FGF15/19 signaling. Similar effects are observed in mice treated with engineered Escherichia coli Nissle 1917 that are capable of expressing bile acid 7α-dehydratas (BaiE) from C. scindens (EcN-BaiE). Activating intestinal FXR-FGF15/19 signaling by fexaramine (Fex) or recombinant protein FGF19 reverse vancomycin-induced liver injury and fibrosis. These results demonstrate that long-term oral vancomycin exacerbates cholestatic liver injury, while C. scindens mitigates this effect by activating the intestinal FXR-FGF15/19 signaling pathway. This underscores the importance of monitoring bile acid levels in PSC patients receiving vancomycin treatment and suggests that C. scindens may serve as a potential therapeutic approach for PSC patients.

Indexed as

CholestasisClostridiumFibroblast Growth FactorsLiver CirrhosisReceptors, Cytoplasmic and NuclearVancomycinAnimalsAnti-Bacterial AgentsBile Acids and SaltsGastrointestinal MicrobiomeHumansMaleMiceMice, Inbred C57BLReceptor, Farnesoid X-ActivatedSignal TransductionAnti-Bacterial AgentsBile Acids and Saltsfibroblast growth factor 15, mouseFibroblast Growth FactorsReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearVancomycincholestatic liver diseasesClostridium scindensFXR‐FGF15/19 signalinggut microbiotaliver fibrosisvancomycin

Identifiers

PMID39680750
PMCPMC11791999

What OpenQuestion holds

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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.