Evidence map›Paper›PMID 41321495›Full record

ArticleFrontiers in physiology2025

Activation of the pentose phosphate pathway by microcurrent stimulation mediates antioxidant effects in inflammation-stimulated macrophages.

Mikiko Uemura, Noriaki Maeshige, Atomu Yamaguchi, Xiaoqi Ma, Yunfei Fu, Taketo Inoue, Mami Matsuda, Yuya Nishimura, Tomohisa Hasunuma, Ji Wang and 2 more

Abstract read
In one paragraph

Article in Frontiers in physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

12 authors.

Mikiko UemuraDepartment of Rehabilitation Science, Kobe University Graduate School of Health Sciences, Kobe, Japan.
Noriaki Maeshige *Department of Rehabilitation Science, Kobe University Graduate School of Health Sciences, Kobe, Japan.
Atomu Yamaguchi *Department of Rehabilitation Science, Kobe University Graduate School of Health Sciences, Kobe, Japan.
Xiaoqi Ma *Department of Rehabilitation Science, Kobe University Graduate School of Health Sciences, Kobe, Japan.
Yunfei Fu *Department of Rehabilitation Science, Kobe University Graduate School of Health Sciences, Kobe, Japan.
Taketo Inoue *Department of Rehabilitation Science, Kobe University Graduate School of Health Sciences, Kobe, Japan.
Mami Matsuda *Graduate School of Science, Technology and Innovation, Kobe University, Kobe, Japan.
Yuya Nishimura *Graduate School of Science, Technology and Innovation, Kobe University, Kobe, Japan.
Tomohisa Hasunuma *Graduate School of Science, Technology and Innovation, Kobe University, Kobe, Japan.
Ji Wang *Department of Toxicology and Sanitary Chemistry, School of Public Health, Capital Medical University, Beijing, China.
Hiroyo Kondo *Department of Nutrition, Faculty of Health and Nutrition, Shubun University, Ichinomiya, Aichi, Japan.
Hidemi FujinoDepartment of Rehabilitation Science, Kobe University Graduate School of Health Sciences, Kobe, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Excessive inflammatory responses in macrophages lead to increased oxidative stress, and the excessive production of reactive oxygen species (ROS) causes tissue damage, contributing to the development of chronic diseases and tissue deterioration. Therefore, controlling the inflammatory response and ROS production is crucial for human health. Electrical stimulation (ES) has been shown to have antioxidant and anti-inflammatory effects on macrophages. However, the key pathway underlying these effects remains unclear. Methods: In this study, ES was applied to Lipopolysaccharide (LPS)-stimulated macrophages, and the production of ROS and 8-hydroxy-2'-deoxyguanosine (8-OHdG), inflammatory cytokine expression, and intracellular metabolites were analyzed in a glucose-6-phosphate dehydrogenase (G6PD) knockdown experiment, the rate-limiting enzyme of the Pentose Phosphate Pathway(PPP). Results: ES significantly increased sedoheptulose 7-phosphate (S7P), an intermediate metabolite in PPP, and reduced ROS and 8-OHdG production and the expression of inflammatory cytokines in LPS-stimulated macrophages. Meanwhile, ES did not exert antioxidant effects in G6PD-knockdown macrophages. Discussion: These findings indicate that the antioxidant effects of ES are mediated by PPP in LPS-stimulated macrophages.

Indexed as

glucose metabolismmacrophagemicrocurrent stimulationNADPHoxidative stresspentose phosphate pathway (PPP)

Identifiers

PMID41321495
PMCPMC12660068

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.