Evidence map›Paper›PMID 35212163›Full record

ArticlePharmacology research & perspectives2022

2-Deoxy-d-glucose induces deglycosylation of proinflammatory cytokine receptors and strongly reduces immunological responses in mouse models of inflammation.

Ikuno Uehara, Mitsuko Kajita, Atsuko Tanimura, Shigeaki Hida, Munehiko Onda, Zenya Naito, Shinsuke Taki, Nobuyuki Tanaka

Open access · goldAbstract read
In one paragraph

Article in Pharmacology research & perspectives, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

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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 4 institutions in 1 country.

Ikuno UeharaDepartment of Molecular Oncology, Institute for Advanced Medical Sciences, Nippon Medical School, Tokyo, Japan.
Mitsuko KajitaDepartment of Molecular Oncology, Institute for Advanced Medical Sciences, Nippon Medical School, Tokyo, Japan.
Atsuko TanimuraDepartment of Molecular Oncology, Institute for Advanced Medical Sciences, Nippon Medical School, Tokyo, Japan.
Shigeaki HidaDepartment of Molecular and Cellular Health Sciences, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya, Japan.
Munehiko OndaDepartment of Pathology, Integrative Oncological Pathology, Nippon Medical School, Tokyo, Japan.
Zenya NaitoDepartment of Pathology, Integrative Oncological Pathology, Nippon Medical School, Tokyo, Japan.
Shinsuke TakiDepartment of Molecular and Cellular Immunology, Shinshu University School of Medicine, Matsumoto, Japan.
Nobuyuki TanakaDepartment of Molecular Oncology, Institute for Advanced Medical Sciences, Nippon Medical School, Tokyo, Japan.ORCID 0000-0002-6373-2220
Nippon Medical School · JPNippon Medical School Hospital · JPNagoya City University · JPShinshu University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Anti-proinflammatory cytokine therapies against interleukin (IL)-6, tumor necrosis factor (TNF)-α, and IL-1 are major advancements in treating inflammatory diseases, especially rheumatoid arthritis. Such therapies are mainly performed by injection of antibodies against cytokines or cytokine receptors. We initially found that the glycolytic inhibitor 2-deoxy-d-glucose (2-DG), a simple monosaccharide, attenuated cellular responses to IL-6 by inhibiting N-linked glycosylation of the IL-6 receptor gp130. Aglycoforms of gp130 did not bind to IL-6 or activate downstream intracellular signals that included Janus kinases. 2-DG completely inhibited dextran sodium sulfate-induced colitis, a mouse model for inflammatory bowel disease, and alleviated laminarin-induced arthritis in the SKG mouse, an experimental model for human rheumatoid arthritis. These diseases have been shown to be partially dependent on IL-6. We also found that 2-DG inhibited signals for other proinflammatory cytokines such as TNF-α, IL-1β, and interferon -γ, and accordingly, prevented death by another inflammatory disease, lipopolysaccharide (LPS) shock. Furthermore, 2-DG prevented LPS shock, a model for a cytokine storm, and LPS-induced pulmonary inflammation, a model for acute respiratory distress syndrome of coronavirus disease 2019 (COVID-19). These results suggest that targeted therapies that inhibit cytokine receptor glycosylation are effective for treatment of various inflammatory diseases.

Indexed as

AnimalsAnti-Inflammatory Agents, Non-SteroidalCells, CulturedCytokine Receptor gp130Cytokine Release SyndromeCytokinesDeoxyglucoseGlycosylationInflammationJanus KinasesLipopolysaccharidesMiceMice, Inbred C57BLMice, KnockoutReceptors, CytokineReceptors, Interleukin-6Anti-Inflammatory Agents, Non-SteroidalCytokine Receptor gp130CytokinesDeoxyglucoseIl6ra protein, mouseIl6st protein, mouseJanus KinasesLipopolysaccharidesReceptors, CytokineReceptors, Interleukin-62-Deoxy-d-glucose (2-DG)cytokine stormdeglycosylationinflammatory bowel diseaseinflammatory diseasesproinflammatory cytokine receptorsrheumatoid arthritis

Identifiers

PMID35212163
PMCPMC8873284
OpenAlexW4214628987

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.