Evidence map›Paper›PMID 38727823›Full record

ArticleJournal of gastroenterology2024

High-mobility group box 1 fragment ameliorates chronic pancreatitis induced by caerulein in mice.

Daiki Hokkoku, Kazuki Sasaki, Shogo Kobayashi, Takashi Shimbo, Tomomi Kitayama, Sho Yamazaki, Yukari Yamamoto, Yuya Ouchi, Hiroki Imamura, Takeshi Kado and 10 more

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of gastroenterology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. HMGB1: key mediator in digestive system diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
  5. Article
  6. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

20 authors.

Daiki HokkokuDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka E-2, Suita, Osaka, 565-0871, Japan.
Kazuki SasakiDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka E-2, Suita, Osaka, 565-0871, Japan.
Shogo KobayashiDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka E-2, Suita, Osaka, 565-0871, Japan. skobayashi@gesurg.med.osaka-u.ac.jp.ORCID 0000-0002-8828-1067
Takashi ShimboDepartment of Stem Cell Therapy Science, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.
Tomomi KitayamaDepartment of Stem Cell Therapy Science, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.
Sho YamazakiDepartment of Stem Cell Therapy Science, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.
Yukari YamamotoDepartment of Stem Cell Therapy Science, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.
Yuya OuchiDepartment of Stem Cell Therapy Science, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.
Hiroki ImamuraDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka E-2, Suita, Osaka, 565-0871, Japan.
Takeshi KadoDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka E-2, Suita, Osaka, 565-0871, Japan.
Keisuke ToyaDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka E-2, Suita, Osaka, 565-0871, Japan.
Wataru FujiiDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka E-2, Suita, Osaka, 565-0871, Japan.
Yoshifumi IwagamiDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka E-2, Suita, Osaka, 565-0871, Japan.
Daisaku YamadaDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka E-2, Suita, Osaka, 565-0871, Japan.
Yoshito TomimaruDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka E-2, Suita, Osaka, 565-0871, Japan.
Takehiro NodaDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka E-2, Suita, Osaka, 565-0871, Japan.
Hidenori TakahashiDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka E-2, Suita, Osaka, 565-0871, Japan.
Katsuto TamaiDepartment of Stem Cell Therapy Science, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.
Yuichiro DokiDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka E-2, Suita, Osaka, 565-0871, Japan.
Hidetoshi EguchiDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka E-2, Suita, Osaka, 565-0871, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChronic pancreatitis (CP) is a progressive disease characterized by pancreatic fibrosis for which effective treatment options are lacking. Mesenchymal stem cells (MSCs) have shown potential for fibrosis treatment but face limitations in clinical application. The high-mobility group box 1 (HMGB1) fragment mobilizes MSCs from bone marrow into the blood and has emerged as a promising therapeutic agent for tissue regeneration in various pathological conditions. The aim of this study was to investigate the potential therapeutic effects of systemic administration of the HMGB1 fragment in a mouse model of CP.

methodsA caerulein-induced CP mouse model was used, and the HMGB1 fragment was administered by tail vein injection. Parameters such as body weight, pancreatic tissue damage, fibrosis, inflammatory cytokine expression, and collagen-related gene expression were evaluated using various assays, including immunohistochemistry, real-time PCR, serum analysis, and single-cell transcriptome analysis. And the migration of MSCs to the pancreas was evaluated using the parabiosis model.

resultsAdministration of the HMGB1 fragment was associated with significant improvements in pancreatic tissue damage and fibrosis. It suppressed the expression of inflammatory cytokines and activated platelet-derived growth factor receptor-α

conclusionThese findings highlight the potential of the HMGB1 fragment as a therapeutic target for the treatment of CP.

Indexed as

CeruletideDisease Models, AnimalFibrosisHMGB1 ProteinPancreasPancreatitis, ChronicAnimalsCytokinesMaleMesenchymal Stem CellsMesenchymal Stem Cell TransplantationMiceMice, Inbred C57BLCeruletideCytokinesHMGB1 ProteinHMGB1 protein, mouseChronic pancreatitisHigh-mobility group box 1Mesenchymal stem cellPancreas

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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.