Evidence map›Paper›PMID 42470108›Full record

ArticleGut microbes2026

Yan Cheng, Zhanxuan E Wu, Ruoyue Huang, Qingmei Li, Dongmei Yan, Yuqi Chen, WeiFeng Zhu, Fei Li

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

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

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

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

8 authors.

Yan ChengDepartment of Gastroenterology & Hepatology, Laboratory of Hepato-intestinal Diseases and Metabolism, Frontiers Science Center for Disease-related Molecular Network, West China Hospital, Sichuan University, Chengdu, China.ORCID 0009-0006-6050-6187
Zhanxuan E WuDepartment of Gastroenterology & Hepatology, Laboratory of Hepato-intestinal Diseases and Metabolism, Frontiers Science Center for Disease-related Molecular Network, West China Hospital, Sichuan University, Chengdu, China.
Ruoyue HuangDepartment of Gastroenterology & Hepatology, Laboratory of Hepato-intestinal Diseases and Metabolism, Frontiers Science Center for Disease-related Molecular Network, West China Hospital, Sichuan University, Chengdu, China.
Qingmei LiDepartment of Gastroenterology & Hepatology, Laboratory of Hepato-intestinal Diseases and Metabolism, Frontiers Science Center for Disease-related Molecular Network, West China Hospital, Sichuan University, Chengdu, China.
Dongmei YanAcademician Workstation, Jiangxi University of Chinese Medicine, Nanchang, China.
Yuqi ChenDepartment of Gastroenterology & Hepatology, Laboratory of Hepato-intestinal Diseases and Metabolism, Frontiers Science Center for Disease-related Molecular Network, West China Hospital, Sichuan University, Chengdu, China.
WeiFeng ZhuSchool of Pharmacy, Jiangxi University of Chinese Medicine, Nanchang, China.
Fei LiDepartment of Gastroenterology & Hepatology, Laboratory of Hepato-intestinal Diseases and Metabolism, Frontiers Science Center for Disease-related Molecular Network, West China Hospital, Sichuan University, Chengdu, China.ORCID 0000-0001-6911-2033

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ulcerative colitis (UC) is a systemic disease that can involve multiple organs, and hepatobiliary diseases in UC patients are frequently observed. However, the pathogenesis of UC and its associated hepatobiliary complications remains elusive, and limited therapeutic options are available. This study revealed that disrupted hepatic lipid metabolism plays a pivotal role in driving the progression of UC and its extraintestinal hepatobiliary manifestations. Mechanistically, colitis-elevated circulating endogenous corticosterone (CORT) mediates the downregulation of hepatic LXRα-SCD1 signaling, resulting in diminished monounsaturated fatty acid (MUFA), reduced unsaturated lysophospholipids, and the accumulation of alkyl lysophospholipids, ceramide and hexosylceramide. These alterations contribute to liver lipotoxicity and, in turn, exacerbate colitis. A similar lipid profile is observed in UC patients. Importantly, pristimerin, a natural compound structurally similar to the star molecule celastrol, has been demonstrated to alleviate UC and concomitant liver injury by remodeling hepatic lipid metabolism in a microbiota-dependent manner. The gut commensal

Indexed as

Colitis, UlcerativeLactobacillus johnsoniiLipid MetabolismLiver X ReceptorsStearoyl-CoA DesaturaseTriterpenesAnimalsGastrointestinal MicrobiomeHumansLiverMaleMiceMice, Inbred C57BLPentacyclic TriterpenesSignal TransductioncelastrolLiver X ReceptorsNr1h3 protein, mousePentacyclic TriterpenesStearoyl-CoA DesaturaseTriterpenesgut–liver axisLactobacillus johnsoniiliver injurypristimerinulcerative colitis

Identifiers

PMID42470108
PMCPMC13387113

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.