Evidence map›Paper›PMID 40548381›Full record

ArticleJCI insight2025

Type 2 diabetes alters quiescent pancreatic stellate cells to tumor-prone state.

Yutaro Hara, Hiroki Mizukami, Takahiro Yamada, Shuji Shimoyama, Keisuke Yamazaki, Takanori Sasaki, Zhenchao Wang, Hanae Kushibiki, Masaki Ryuzaki, Saori Ogasawara and 6 more

Abstract read
In one paragraph

Article in JCI insight, 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

16 authors.

Yutaro HaraDepartment of Pathology and Molecular Medicine, Biomedical Research Center.
Hiroki MizukamiDepartment of Pathology and Molecular Medicine, Biomedical Research Center.
Takahiro YamadaDepartment of Pathology and Molecular Medicine, Biomedical Research Center.
Shuji ShimoyamaDepartment of Neurophysiology, Biomedical Research Center, Hirosaki University, Hirosaki, Japan.
Keisuke YamazakiDepartment of Pathology and Molecular Medicine, Biomedical Research Center.
Takanori SasakiDepartment of Pathology and Molecular Medicine, Biomedical Research Center.
Zhenchao WangDepartment of Pathology and Molecular Medicine, Biomedical Research Center.
Hanae KushibikiDepartment of Pathology and Molecular Medicine, Biomedical Research Center.
Masaki RyuzakiDepartment of Pathology and Molecular Medicine, Biomedical Research Center.
Saori OgasawaraDepartment of Pathology and Molecular Medicine, Biomedical Research Center.
Hiroaki TambaDepartment of Pathology and Molecular Medicine, Biomedical Research Center.
Akiko ItayaDepartment of Pathology and Molecular Medicine, Biomedical Research Center.
Norihisa KimuraDepartment of Gastroenterological Surgery, and.
Keinosuke IshidoDepartment of Gastroenterological Surgery, and.
Shinya UenoDepartment of Neurophysiology, Biomedical Research Center, Hirosaki University, Hirosaki, Japan.
Kenichi HakamadaDepartment of Gastroenterological Surgery, and.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic stellate cells (PSCs) are the origin of cancer-associated fibroblasts. Type 2 diabetes mellitus (T2D) may promote pancreatic ductal adenocarcinoma (PDAC), eliciting changes in the quiescent PSC (qPSC) population from the precancerous stage. However, the details are unknown. We evaluated the subpopulations of qPSCs and the impact of T2D. PSCs isolated from 8-week-old C57BL/6J mice and diabetic db/db mice were analyzed by single-cell RNA-seq. Sorted qPSCs and PDAC cells were transplanted into allogenic mice. The isolated qPSCs were broadly classified into mesothelial cell and pancreatic fibroblast (Paf) populations by single-cell RNA-seq. Pafs were subclassified into inflammatory Pafs, myofibroblastic Pafs (myPafs) and a small population named tumor immunity- and angiogenesis-promoting Pafs (tapPafs), expressing Cxcl13. In the subcutaneous transplantation model, the tumors transplanted with myPafs were significantly larger than the tumors transplanted with tapPafs. An increase in myPafs and a decrease in tapPafs were observed from the precancerous stage in human T2D, indicating the effects of tumor progression. This study revealed the subpopulation changes in qPSCs in T2D. A therapy that increases the number of tapPafs could be a therapeutic option for patients with PDAC and T2D and even those in a precancerous stage of T2D.

Indexed as

Carcinoma, Pancreatic DuctalDiabetes Mellitus, Type 2Pancreatic NeoplasmsPancreatic Stellate CellsAnimalsCancer-Associated FibroblastsDisease Models, AnimalHumansMaleMiceMice, Inbred C57BLCancerDiabetesEndocrinologyFibrosisGastroenterology

Identifiers

PMID40548381
PMCPMC12220947

What OpenQuestion holds

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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.