Evidence map›Paper›PMID 41431138›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026

Hepatocyte Mettl3 Deficiency Drives Primary Sclerosing Cholangitis and Liver Fibrosis via Cholangiocyte-Macrophage Crosstalk.

Wenting Pan, Yuting Yong, Yuanshuai Li, Gaona Shi, Min Zhang, Lingfei Wan, Yue Zhao, Wenling Zhan, Yanli Lin, Qiaozhen Qin and 10 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. RNA mActa pharmacologica Sinica · 2026
    Review
  2. Article
  3. Review
  4. Article
  5. 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

20 authors.

Wenting PanBeijing Key Laboratory of Environmental and Viral Oncology, College of Chemistry and Life Science, Beijing University of Technology, Beijing, China.
Yuting YongBeijing Key Laboratory of Environmental and Viral Oncology, College of Chemistry and Life Science, Beijing University of Technology, Beijing, China.
Yuanshuai LiBeijing Key Laboratory of Environmental and Viral Oncology, College of Chemistry and Life Science, Beijing University of Technology, Beijing, China.
Gaona ShiState Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Min ZhangDepartment of Nephrology, First Medical Center, Chinese PLA General Hospital, Beijing, China.
Lingfei WanBeijing Key Laboratory of Environmental and Viral Oncology, College of Chemistry and Life Science, Beijing University of Technology, Beijing, China.
Yue ZhaoBeijing Key Laboratory of Environmental and Viral Oncology, College of Chemistry and Life Science, Beijing University of Technology, Beijing, China.
Wenling ZhanBeijing Key Laboratory of Environmental and Viral Oncology, College of Chemistry and Life Science, Beijing University of Technology, Beijing, China.
Yanli LinLaboratory of Advanced Biotechnology, Beijing Institute of Biotechnology, Beijing, China.
Qiaozhen QinBeijing Key Laboratory of Environmental and Viral Oncology, College of Chemistry and Life Science, Beijing University of Technology, Beijing, China.
Xupeng ChenBeijing Key Laboratory of Environmental and Viral Oncology, College of Chemistry and Life Science, Beijing University of Technology, Beijing, China.
Yanli NiState Key Laboratory of Experimental Hematology, Institute of Hematology, Senior Department of Hematology, Fifth Medical Center, Chinese PLA General Hospital, Beijing, China.
Haixu ChenInstitute of Geriatrics &National Clinical Research Center of Geriatrics Disease, the Second Medical Center, Chinese PLA General Hospital, Beijing, China.
Wenzai ShiDepartment of Hepatobiliary Surgery, Peking University International Hospital, Beijing, China.
Xiaomeng GuoBeijing Key Laboratory of Environmental and Viral Oncology, College of Chemistry and Life Science, Beijing University of Technology, Beijing, China.
Juan ChenKey Laboratory of Precision Nutrition and Food Quality, Department of Nutrition and Health, China Agricultural University, Beijing, China.
Shuchen LiuBeijing Institute of Radiation Medicine, Beijing, China.
Youliang WangLaboratory of Advanced Biotechnology, Beijing Institute of Biotechnology, Beijing, China.
Bing LiuState Key Laboratory of Experimental Hematology, Institute of Hematology, Senior Department of Hematology, Fifth Medical Center, Chinese PLA General Hospital, Beijing, China.
Xinlong YanBeijing Key Laboratory of Environmental and Viral Oncology, College of Chemistry and Life Science, Beijing University of Technology, Beijing, China.ORCID https://orcid.org/0000-0001-9967-5654

Funding

National Natural Science Foundation of China 82173183National Natural Science Foundation of China 82203636National Natural Science Foundation of China 82271628National Natural Science Foundation of China 82470115R&D program of Beijing Municipal Education Commission KZ202210005010The Fundamental Research Funds for Beijing Municipal Universities 05500054625503
6 · The paper itself

Abstract

Effective therapies for primary sclerosing cholangitis (PSC), a progressive cholestatic liver disease characterized by biliary inflammation and fibrotic damage, remain limited due to an incomplete elucidation of its underlying molecular mechanisms. Although N6-methyladenosine (m6A) RNA methylation has been implicated in hepatic pathophysiology, its role in PSC remains undefined. Here, we demonstrate that hepatocyte-specific deletion of Mettl3, a critical m6A methyltransferase, induces spontaneous PSC-like pathology characterized by ductular reaction and peribiliary fibrosis. Therapeutic restoration of Mettl3 through genetic knock-in or AAV8-mediated hepatocyte-specific overexpression significantly attenuated 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC)-induced PSC progression. Integrated single-cell and bulk transcriptomic profiles revealed an expansion of Trem2

Indexed as

Cholangitis, SclerosingHepatocytesLiver CirrhosisMacrophagesMethyltransferasesAnimalsDisease Models, AnimalHumansMiceMice, Inbred C57BLMice, KnockoutMethyltransferasesMettl3 protein, mouseliver fibrosisMettl3primary sclerosing cholangitisSpp1+ cholangiocyteTrem2+ macrophage

Identifiers

PMID41431138
PMCPMC12955918

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.