Evidence map›Paper›PMID 36477360›Full record

ArticleJCI insight2022

RAGE activation in macrophages and development of experimental diabetic polyneuropathy.

Sho Osonoi, Hiroki Mizukami, Yuki Takeuchi, Hikari Sugawa, Saori Ogasawara, Shizuka Takaku, Takanori Sasaki, Kazuhiro Kudoh, Koichi Ito, Kazunori Sango and 5 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

31 citing papers in PubMed, 37 citations in OpenAlex.

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  11. The interaction between oxidative stress and Schwann cells.Experimental biology and medicine (Maywood, N.J.) · 2026
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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

15 authors at 5 institutions in 1 country.

Sho OsonoiDepartment of Pathology and Molecular Medicine and.
Hiroki MizukamiDepartment of Pathology and Molecular Medicine and.
Yuki TakeuchiDepartment of Pathology and Molecular Medicine and.
Hikari SugawaLaboratory of Food and Regulation Biology, Department of Bioscience, School of Agriculture, Tokai University, Higashi-ku, Kumamoto, Japan.
Saori OgasawaraDepartment of Pathology and Molecular Medicine and.
Shizuka TakakuDiabetic Neuropathy Project, Department of Diseases and Infection, Tokyo Metropolitan Institute of Medical Science, Setagaya-ku, Tokyo, Japan.
Takanori SasakiDepartment of Pathology and Molecular Medicine and.
Kazuhiro KudohDepartment of Pathology and Molecular Medicine and.
Koichi ItoDepartment of Bioscience and Laboratory Medicine, Hirosaki University Graduate School of Health Sciences, Hirosaki, Japan.
Kazunori SangoDiabetic Neuropathy Project, Department of Diseases and Infection, Tokyo Metropolitan Institute of Medical Science, Setagaya-ku, Tokyo, Japan.
Ryoji NagaiLaboratory of Food and Regulation Biology, Department of Bioscience, School of Agriculture, Tokai University, Higashi-ku, Kumamoto, Japan.
Yasuhiko YamamotoDepartment of Biochemistry and Molecular Vascular Biology, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Japan.
Makoto DaimonDepartment of Endocrinology and Metabolism, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Hiroshi YamamotoKomatsu University, Komatsu, Japan.
Soroku YagihashiDepartment of Pathology and Molecular Medicine and.
Hirosaki University · JPKyushu Tokai University · JPTokyo Metropolitan Institute of Medical Science · JPKanazawa University · JPKomatsu University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is suggested that activation of receptor for advanced glycation end products (RAGE) induces proinflammatory response in diabetic nerve tissues. Macrophage infiltration is invoked in the pathogenesis of diabetic polyneuropathy (DPN), while the association between macrophage and RAGE activation and the downstream effects of macrophages remain to be fully clarified in DPN. This study explored the role of RAGE in the pathogenesis of DPN through the modified macrophages. Infiltrating proinflammatory macrophages impaired insulin sensitivity, atrophied the neurons in dorsal root ganglion, and slowed retrograde axonal transport (RAT) in the sciatic nerve of type 1 diabetic mice. RAGE-null mice showed an increase in the population of antiinflammatory macrophages, accompanied by intact insulin sensitivity, normalized ganglion cells, and RAT. BM transplantation from RAGE-null mice to diabetic mice protected the peripheral nerve deficits, suggesting that RAGE is a major determinant for the polarity of macrophages in DPN. In vitro coculture analyses revealed proinflammatory macrophage-elicited insulin resistance in the primary neuronal cells isolated from dorsal root ganglia. Applying time-lapse recording disclosed a direct impact of proinflammatory macrophage and insulin resistance on the RAT deficits in primary neuronal cultures. These results provide a potentially novel insight into the development of RAGE-related DPN.

Indexed as

Diabetes Mellitus, ExperimentalDiabetic NeuropathiesInsulin ResistanceAnimalsMacrophagesMiceReceptor for Advanced Glycation End ProductsReceptor for Advanced Glycation End ProductsDiabetesEndocrinologyNeurodegenerationNeuroendocrine regulationNeuroscience

Identifiers

PMID36477360
PMCPMC9746912
OpenAlexW4311829226

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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.