Evidence map›Paper›PMID 39905730›Full record

ArticleMolecular therapy : the journal of the American Society of Gene Therapy2025

The deubiquitinase USP28 maintains the expression of PPARγ and its inactivation protects mice from diet-induced MASH and hepatocarcinoma.

Changzhou Cai, Hangqi Luo, Jin Peng, Xinghua Zhen, Xiang Shen, Xiaomei Xi, Jianrong Zhu, Yanfei Fang, Xiaoli Chen, Jiewei Wang and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2025. 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

13 authors.

Changzhou CaiDepartment of Gastroenterology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China; Department of Gastroenterology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou 310016, China.
Hangqi LuoInstitute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou 310058, China.
Jin PengZhejiang Provincial Key Laboratory of Pancreatic Disease, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China.
Xinghua ZhenInstitute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou 310058, China.
Xiang ShenChaser Therapeutics, Inc., Hangzhou, Zhejiang 310018, China.
Xiaomei XiChaser Therapeutics, Inc., Hangzhou, Zhejiang 310018, China.
Jianrong ZhuChaser Therapeutics, Inc., Hangzhou, Zhejiang 310018, China.
Yanfei FangDepartment of Gastroenterology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou 310016, China.
Xiaoli ChenDepartment of Gastroenterology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou 310016, China.
Jiewei WangDepartment of Gastroenterology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China.
Chaohui YuDepartment of Gastroenterology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China. Electronic address: zyyyych@zju.edu.cn.
Pumin ZhangInstitute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou 310058, China; Zhejiang Provincial Key Laboratory of Pancreatic Disease, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China; Cancer Center, Zhejiang University, Hangzhou 310058, China. Electronic address: pzhangbcm@zju.edu.cn.
Chengfu XuDepartment of Gastroenterology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China. Electronic address: xiaofu@zju.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic dysfunction-associated steatohepatitis (MASH), a progressive form of metabolic dysfunction-associated fatty liver disease (MAFLD), is a leading cause of liver disease worldwide and can progress to cirrhosis and cancer. Despite its prevalence, the pathogenesis of MASH remains poorly understood, and there is only one U.S. Food and Drug Administration-approved treatment, highlighting the need for new therapeutic strategies. Peroxisome proliferator-activated receptor (PPAR)γ is activated in the liver under high-fat or obese conditions, promoting lipid storage and contributing to MASH progression. We found that USP28 expression is elevated in the livers of MAFLD/MASH patients. Through dietary induction, including a methionine-choline deficient (MCD) diet and a western diet (WD) combined with carbon tetrachloride (CCl

Indexed as

Carcinoma, HepatocellularFatty LiverLiver NeoplasmsPPAR gammaUbiquitin ThiolesteraseAnimalsDiet, WesternDisease Models, AnimalHumansLiverMaleMethionineMiceSignal TransductionMethioninePPAR gammaUbiquitin Thiolesterasedeubiquitinasehepatocellular carcinomametabolic dysfunction-associated fatty liver diseasemetabolic dysfunction-associated steatohepatitisPPARγUSP28

Identifiers

PMID39905730
PMCPMC11997470

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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.