Evidence map›Paper›PMID 38334676›Full record

ArticleCells2024

Imeglimin Exhibits Novel Anti-Inflammatory Effects on High-Glucose-Stimulated Mouse Microglia through ULK1-Mediated Suppression of the TXNIP-NLRP3 Axis.

Hisashi Kato, Kaori Iwashita, Masayo Iwasa, Sayaka Kato, Hajime Yamakage, Takayoshi Suganami, Masashi Tanaka, Noriko Satoh-Asahara

Open access · goldAbstract read
In one paragraph

Article in Cells, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

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  12. Gut-Brain Axis: Focus on Sex Differences in Neuroinflammation.International journal of molecular sciences · 2024
    Review
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.

Hisashi KatoDepartment of Endocrinology, Metabolism and Hypertension Research, Clinical Research Institute, NHO Kyoto Medical Center, Kyoto 612-8555, Japan.ORCID 0000-0003-4395-8369
Kaori IwashitaDepartment of Endocrinology, Metabolism and Hypertension Research, Clinical Research Institute, NHO Kyoto Medical Center, Kyoto 612-8555, Japan.
Masayo IwasaDepartment of Endocrinology, Metabolism and Hypertension Research, Clinical Research Institute, NHO Kyoto Medical Center, Kyoto 612-8555, Japan.ORCID 0000-0001-8761-9698
Sayaka KatoDepartment of Endocrinology, Metabolism and Hypertension Research, Clinical Research Institute, NHO Kyoto Medical Center, Kyoto 612-8555, Japan.
Hajime YamakageDepartment of Endocrinology, Metabolism and Hypertension Research, Clinical Research Institute, NHO Kyoto Medical Center, Kyoto 612-8555, Japan.
Takayoshi SuganamiDepartment of Molecular Medicine and Metabolism, Research Institute of Environmental Medicine, Nagoya University, Nagoya 464-8601, Japan.ORCID 0000-0002-1918-0465
Masashi TanakaDepartment of Endocrinology, Metabolism and Hypertension Research, Clinical Research Institute, NHO Kyoto Medical Center, Kyoto 612-8555, Japan.ORCID 0000-0003-0719-8972
Noriko Satoh-AsaharaDepartment of Endocrinology, Metabolism and Hypertension Research, Clinical Research Institute, NHO Kyoto Medical Center, Kyoto 612-8555, Japan.ORCID 0000-0002-8645-3144
Kyoto Medical Center · JPNagoya University · JP

Funding

Japan Society for the Promotion of Science JP21H02835Japan Society for the Promotion of Science JP21K17557Japan Society for the Promotion of Science JP22K07411Japan Society for the Promotion of Science JP22K07456Japan Society for the Promotion of Science JP22K11720Japan Society for the Promotion of Science JP22K19723the National Hospital Organization for collaborative clinical research H29-NHO-01
6 · The paper itself

Abstract

Type 2 diabetes mellitus (T2DM) is an epidemiological risk factor for dementia and has been implicated in multifactorial pathologies, including neuroinflammation. In the present study, we aimed to elucidate the potential anti-inflammatory effects of imeglimin, a novel antidiabetic agent, on high-glucose (HG)-stimulated microglia. Mouse microglial BV2 cells were stimulated with HG in the presence or absence of imeglimin. We examined the effects of imeglimin on the levels of proinflammatory cytokines, intracellular reactive oxygen species (ROS), mitochondrial integrity, and components related to the inflammasome or autophagy pathways in these cells. Our results showed that imeglimin suppressed the HG-induced production of interleukin-1beta (IL-1β) by reducing the intracellular ROS levels, ameliorating mitochondrial dysfunction, and inhibiting the activation of the thioredoxin-interacting protein (TXNIP)-NOD-like receptor family pyrin domain containing 3 (NLRP3) axis. Moreover, the inhibitory effects of imeglimin on the TXNIP-NLRP3 axis depended on the imeglimin-induced activation of ULK1, which also exhibited novel anti-inflammatory effects without autophagy induction. These findings suggest that imeglimin exerted novel suppressive effects on HG-stimulated microglia through the ULK1-TXNIP-NLRP3 axis, and may, thereby, contribute to the development of innovative strategies to prevent T2DM-associated cognitive impairment.

Indexed as

Diabetes Mellitus, Type 2TriazinesAnimalsAnti-Inflammatory AgentsAutophagy-Related Protein-1 HomologCarrier ProteinsGlucoseMiceMicrogliaNLR Family, Pyrin Domain-Containing 3 ProteinReactive Oxygen SpeciesThioredoxinsAnti-Inflammatory AgentsAutophagy-Related Protein-1 HomologCarrier ProteinsGlucoseimegliminNLR Family, Pyrin Domain-Containing 3 ProteinReactive Oxygen SpeciesThioredoxinsTriazinesTxnip protein, mouseUlk1 protein, mousehyperglycemiaimegliminmicroglianeuroinflammationtype 2 diabetes mellitusULK1

Identifiers

PMID38334676
PMCPMC10854746
OpenAlexW4391531729

What OpenQuestion holds

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LicenceCC BY
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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.