Evidence map›Paper›PMID 32275672›Full record

ArticlePloS one2020

High-mobility group box 1 fragment suppresses adverse post-infarction remodeling by recruiting PDGFRα-positive bone marrow cells.

Takasumi Goto, Shigeru Miyagawa, Katsuto Tamai, Ryohei Matsuura, Takashi Kido, Toru Kuratani, Kazuo Shimamura, Ryoto Sakaniwa, Akima Harada, Yoshiki Sawa

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.3field-weighted citation impact, top 12% of its field
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

16 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
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  4. PdgfrαGenes & diseases · 2025
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  15. Investigational Treatments for Epidermolysis Bullosa.American journal of clinical dermatology · 2021
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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

10 authors at 1 institution in 1 country.

Takasumi GotoDepartment of Cardiovascular Surgery, Osaka University Graduate School of Medicine, Osaka, Japan.ORCID 0000-0002-4284-9286
Shigeru MiyagawaDepartment of Cardiovascular Surgery, Osaka University Graduate School of Medicine, Osaka, Japan.
Katsuto TamaiDepartment of Stem Cell Therapy Science, Osaka University Graduate School of Medicine, Osaka, Japan.
Ryohei MatsuuraDepartment of Cardiovascular Surgery, Osaka University Graduate School of Medicine, Osaka, Japan.
Takashi KidoDepartment of Cardiovascular Surgery, Osaka University Graduate School of Medicine, Osaka, Japan.
Toru KurataniDepartment of Minimally Invasive Cardiovascular Medicine, Osaka University Graduate School of Medicine, Osaka, Japan.
Kazuo ShimamuraDepartment of Minimally Invasive Cardiovascular Medicine, Osaka University Graduate School of Medicine, Osaka, Japan.
Ryoto SakaniwaDepartment of Social Medicine, Osaka University Graduate School of Medicine, Osaka, Japan.
Akima HaradaDepartment of Cardiovascular Surgery, Osaka University Graduate School of Medicine, Osaka, Japan.
Yoshiki SawaDepartment of Cardiovascular Surgery, Osaka University Graduate School of Medicine, Osaka, Japan.
The University of Osaka · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesHigh-mobility group box 1 protein (HMGB1) fragment enhances bone marrow-derived mesenchymal stem cell (BM-MSC) recruitment to damaged tissue to promote tissue regeneration. This study aimed to evaluate whether systemic injection of HMGB1 fragment could promote tissue repair in a rat model of myocardial infarction (MI).

methodsHMGB1 (n = 14) or phosphate buffered saline (n = 12, control) was administered to MI rats for 4 days. Cardiac performance and left ventricular remodeling were evaluated using ultrasonography and immunostaining. BM-MSC recruitment to damaged tissue in green fluorescent protein-bone marrow transplantation (GFP-BMT) models was evaluated using immunostaining.

resultsAt four weeks post-treatment, the left ventricular ejection fraction was significantly improved in the HMGB1 group compared to that in the control. Interstitial fibrosis and cardiomyocyte hypertrophy were also significantly attenuated in the HMGB1 group compared to the control. In the peri-infarction area, VEGF-A mRNA expression was significantly higher and TGFβ expression was significantly attenuated in the HMGB1 group than in the control. In GFP-BMT rats, GFP+/PDGFRα+ cells were significantly mobilized to the peri-infarction area in the HMGB1 group compared to that in the control, leading to the formation of new vasculature. In addition, intravital imaging revealed that more GFP+/PDGFRα+ cells were recruited to the peri-infarction area in the HMGB1 group than in the control 12 h after treatment.

conclusionsSystemic administration of HMGB1 induced angiogenesis and reduced fibrosis by recruiting PDGFRα+ mesenchymal cells from the bone marrow, suggesting that HMGB1 administration might be a new therapeutic approach for heart failure after MI.

Indexed as

Angiogenesis Inducing AgentsAnimalsDisease Models, AnimalFibrosisHeartHeart FailureHMGB1 ProteinMaleMesenchymal Stem CellsMyocardial InfarctionRatsReceptor, Platelet-Derived Growth Factor alphaRegenerationAngiogenesis Inducing AgentsHMGB1 ProteinReceptor, Platelet-Derived Growth Factor alpha

Identifiers

PMID32275672
PMCPMC7147742
OpenAlexW3016204139

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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.