Evidence map›Paper›PMID 40612681›Full record

ArticleInternational journal of biological sciences2025

Protein Arginine Methyltransferase 1-mediated Histone H4R3 Dimethyl Asymmetric enhances Epidermal Growth Factor Receptor signaling to promote Peritoneal Fibrosis.

Hui Chen, Yingfeng Shi, Jinqing Li, Qin Zhong, Xiaoyan Ma, Yan Hu, Yishu Wang, Daofang Jiang, Xialin Li, Shasha Zhang and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of biological sciences, 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. 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

12 authors.

Hui ChenDepartment of Nephrology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Yingfeng ShiDepartment of Nephrology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Jinqing LiDepartment of Nephrology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Qin ZhongDepartment of Nephrology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Xiaoyan MaDepartment of Nephrology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Yan HuDepartment of Nephrology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Yishu WangDepartment of Nephrology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Daofang JiangDepartment of Nephrology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Xialin LiDepartment of Nephrology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Shasha ZhangDepartment of Nephrology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Shougang ZhuangDepartment of Nephrology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Na LiuDepartment of Nephrology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Peritoneal fibrosis (PF) is regarded as one of the major complications of peritoneal dialysis (PD) and is still lack of efficacious clinical interventions to address this issue. Previous publications have indicated that protein arginine methyltransferase 1 (PRMT1) is involved in the pathological process of various diseases. However, the role of PRMT1 in the development of PF remains to be elucidated. In the present study, we demonstrate that PRMT1 is highly expressed in the peritoneum and dialysis effluent of long-term PD patients, and that there is a positive correlation between PRMT1 and the hallmarks of fibrosis in human peritoneal specimens. Our results further demonstrate that the genetic depletion or pharmacological inhibition of PRMT1 has the potential to reduce extracellular matrix deposition and alleviate PF caused by high-glucose peritoneal dialysis fluid (HG-PDF) in murine models. In addition, silencing or pharmacological inhibition of PRMT1 could also reduce the epithelial-to-mesenchymal (EMT) phenotypic change caused by TGF-β1

Indexed as

ErbB ReceptorsHistonesPeritoneal FibrosisProtein-Arginine N-MethyltransferasesAnimalsEpithelial-Mesenchymal TransitionFemaleHumansMaleMiceMice, Inbred C57BLPeritoneal DialysisRepressor ProteinsSignal TransductionErbB ReceptorsHistonesPRMT1 protein, humanProtein-Arginine N-MethyltransferasesRepressor Proteinsasymmetric dimethylation of histone H4 on arginine 3epidermal growth factor receptorperitoneal fibrosisprotein arginine methyl transferase 1

Identifiers

PMID40612681
PMCPMC12223772

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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.