Evidence map›Paper›PMID 30647411›Full record

ArticleMucosal immunology2019

Regulation of HMGB1 release protects chemoradiotherapy-associated mucositis.

Keon-Il Im, Young-Sun Nam, Nayoun Kim, Yunejin Song, Eun-Sol Lee, Jung-Yeon Lim, Young-Woo Jeon, Seok-Goo Cho

Open access · hybridAbstract read
PubMed Publisher
In one paragraph

Article in Mucosal immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed, 29 citations in OpenAlex.

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  6. The Role of the Innate Immune Response in Oral Mucositis Pathogenesis.International journal of molecular sciences · 2023
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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

8 authors at 2 institutions in 1 country.

Keon-Il ImInstitute for Translational Research and Molecular Imaging, Catholic Institutes of Medical Science, Seoul, Korea.
Young-Sun NamInstitute for Translational Research and Molecular Imaging, Catholic Institutes of Medical Science, Seoul, Korea.
Nayoun KimInstitute for Translational Research and Molecular Imaging, Catholic Institutes of Medical Science, Seoul, Korea.
Yunejin SongInstitute for Translational Research and Molecular Imaging, Catholic Institutes of Medical Science, Seoul, Korea.
Eun-Sol LeeInstitute for Translational Research and Molecular Imaging, Catholic Institutes of Medical Science, Seoul, Korea.
Jung-Yeon LimInstitute for Translational Research and Molecular Imaging, Catholic Institutes of Medical Science, Seoul, Korea.
Young-Woo JeonInstitute for Translational Research and Molecular Imaging, Catholic Institutes of Medical Science, Seoul, Korea.
Seok-Goo ChoInstitute for Translational Research and Molecular Imaging, Catholic Institutes of Medical Science, Seoul, Korea. chosg@catholic.ac.kr.
Seoul St. Mary's Hospital · KRCatholic University of Korea · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oral mucositis (OM) is a common complication in cancer patients undergoing anticancer treatment. Despite the clinical and economic consequences of OM, there are no drugs available for its fundamental control. Here we show that high-mobility group box 1 (HMGB1), a "danger signal" that acts as a potent innate immune mediator, plays a critical role in the pathogenesis of OM. In addition, we investigated treatment of OM through HMGB1 blockade using NecroX-7 (tetrahydropyran-4-yl)-[2-phenyl-5-(1,1-dioxo-thiomorpholin-4-yl)methyl-1Hindole-7-yl]amine). NecroX-7 ameliorated basal layer epithelial cell death and ulcer size in OM induced by chemotherapy or radiotherapy. This protective effect of NecroX-7 was mediated by inhibition of HMGB1 release and downregulation of mitochondrial oxidative stress. Additionally, NecroX-7 inhibited the HMGB1-induced release of tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β, and macrophage inflammatory protein (MIP)-1β, as well as the expression of p53-upregulated modulator of apoptosis (PUMA) and the excessive inflammatory microenvironment, including nuclear factor-kB (NF-kB) pathways. In conclusion, our findings suggest that HMGB1 plays a key role in the pathogenesis of OM; therefore, blockade of HMGB1 by NecroX-7 may be a novel therapeutic strategy for OM.

Indexed as

AcetylcysteineAnimalsChemoradiotherapyDisease Models, AnimalFemaleHistonesHMGB1 ProteinHumansMiceMouth MucosaMucositisNeoplasmsNF-kappa BOrganic ChemicalsProtective AgentsProtein TransportAcetylcysteineHistonesHMGB1 Proteinnecrox-7NF-kappa BOrganic ChemicalsProtective AgentsReactive Oxygen SpeciesTumor Suppressor Protein p53

Identifiers

PMID30647411
OpenAlexW2909979785

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.