Evidence map›Paper›PMID 41857463›Full record

ArticleInflammation2026

A Novel Insight into Chronic Pancreatitis Pathogenesis: the USP1/ITGB5 Axis-Mediated Stellate Cell Activation.

Dongyan Wang, Yihai Shi, Jie Lu, Wen Bao, Nan Wang, Qiuteng Shen, Zhenyu Lin, Lijuan Qian, Chang Zhu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Inflammation, 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.

  1. Article
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

9 authors.

Dongyan Wang *School of Gongli Hospital Medical Technology, University of Shanghai for Science and Technology, Shanghai, 200093, China.
Yihai Shi *Department of Gastroenterology, Gongli Hospital of Shanghai Pudong New Area, 219 Miao Pu Road, Shanghai, 200135, China.
Jie LuDepartment of Gastroenterology, First People's Hospital Affiliated to School of Medicine, Shanghai Jiaotong University, 85 Wujin Road, Shanghai, 200080, China.
Wen BaoClinical Research Unit, Institute of Clinical Science, Zhongshan Hospital of Fudan University, Shanghai, 200032, China.
Nan WangDepartment of Gastroenterology, First People's Hospital Affiliated to School of Medicine, Shanghai Jiaotong University, 85 Wujin Road, Shanghai, 200080, China.
Qiuteng ShenSchool of Gongli Hospital Medical Technology, University of Shanghai for Science and Technology, Shanghai, 200093, China.
Zhenyu LinSchool of Gongli Hospital Medical Technology, University of Shanghai for Science and Technology, Shanghai, 200093, China.
Lijuan QianPostgraduate training base at Shanghai Gongli Hospital, Ningxia medical university, Shanghai, 200135, China.
Chang ZhuDepartment of Gastroenterology, Sir Run Run Shaw Hospital, College of Medicine, Zhejiang University, No.3 Qingchun East Road, Shangcheng District, 310016, Hangzhou City, Zhejiang Province, China. 3322141@zju.edu.cn.ORCID http://orcid.org/0009-0006-9116-3922

Funding

Shanghai Municipal Health Commission Clinical Research Special Project of the Health Industry in 2025 20254Y0066The Investigator-initiated Trial Program of Shanghai Pudong New Area Health Commission (the Medical and Industrial Integration Program) 2025-PWYC-04The "Three Navigation" Plan of Talent Training in Pudong New Area Gongli Hospital 2025-GLSHQH-03Zhejiang Traditional Chinese Medicine Science and Technology Plan in 2025 (Young Talents Support Program Project) NO.2025ZR149
6 · The paper itself

Abstract

Chronic pancreatitis (CP) is characterized by chronic pancreatic inflammation and progressive fibrosis. This study investigated the role of ubiquitin-specific peptidase 1 (USP1), a protein-stabilizing deubiquitinase, in CP. C57BL/6J mice were given 8-week repetitive intraperitoneal cerulein (50 µg/kg) injections to establish the CP model. USP1 expression in CP mouse pancreatic tissues was 3-fold higher than in controls. Lentivirus-mediated Usp1 knockdown reduced pancreatic inflammatory cell infiltration, trypsin activity, and proinflammatory cytokine levels. Additionally, Usp1 knockdown inhibits collagen deposition and fibrosis of the pancreas. In vitro, USP1 was upregulated in activated pancreatic stellate cells (PSCs) induced by TGF-β1 (5 ng/mL). USP1 knockdown decreased the expressions of collagen type I alpha 1 chain (COL1A1), COL1A2, fibronectin, and α-smooth muscle actin (α-SMA), suppressing PSC activation and extracellular matrix production. Immunoprecipitation-liquid chromatography/mass spectrometry (IP-LC/MS) and label-free proteomics identified integrin subunit beta 5 (ITGB5) as a potential target protein of USP1. USP1 promoted ITGB5 deubiquitination/stabilization, while USP1 knockdown reduced ITGB5 expression. Rescue experiments showed ITGB5 overexpression reversed the inhibitory effect of USP1 knockdown on PSC activation. Moreover, ITGB5 knockdown inhibited PSC activation via suppressing PI3K/AKT pathway. In conclusion, USP1 knockdown inhibits PSC activation by suppressing the ITGB5-PI3K-AKT axis, thereby alleviating the pathological progression of CP.

Indexed as

Pancreatic Stellate CellsPancreatitis, ChronicUbiquitin-Specific ProteasesAnimalsMaleMiceMice, Inbred C57BLSignal TransductionUbiquitin-Specific ProteasesChronic pancreatitisFibrosisITGB5Pancreatic stellate cellUSP1

Identifiers

PMID41857463
PMCPMC13035630

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.