Evidence map›Paper›PMID 40250557›Full record

ArticleJournal of advanced research2026

Medical gas plasma modifies Nrf2 signaling in diabetic wound healing.

Anke Schmidt, Lea Miebach, Can Bagli, Liane Kantz, Steffen Emmert, Thomas von Woedtke, Sander Bekeschus

Abstract read
In one paragraph

Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
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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

7 authors.

Anke SchmidtZIK Plasmatis, Leibniz Institute for Plasma Science and Technology (INP), a member of the Leibniz Health Research Alliance, Felix-Hausdorff-Str. 2, Greifswald 17489, Germany.
Lea MiebachZIK Plasmatis, Leibniz Institute for Plasma Science and Technology (INP), a member of the Leibniz Health Research Alliance, Felix-Hausdorff-Str. 2, Greifswald 17489, Germany.
Can BagliZIK Plasmatis, Leibniz Institute for Plasma Science and Technology (INP), a member of the Leibniz Health Research Alliance, Felix-Hausdorff-Str. 2, Greifswald 17489, Germany.
Liane KantzZIK Plasmatis, Leibniz Institute for Plasma Science and Technology (INP), a member of the Leibniz Health Research Alliance, Felix-Hausdorff-Str. 2, Greifswald 17489, Germany.
Steffen EmmertDepartment of Dermatology and Venereology, University Medical Center Rostock, Strempelstr. 13, Rostock 18057, Germany.
Thomas von WoedtkeZIK Plasmatis, Leibniz Institute for Plasma Science and Technology (INP), a member of the Leibniz Health Research Alliance, Felix-Hausdorff-Str. 2, Greifswald 17489, Germany; Institute of Hygiene and Environmental Medicine, Greifswald University Medical Center, Sauerbruchstr., Greifswald 17475, Germany.
Sander BekeschusZIK Plasmatis, Leibniz Institute for Plasma Science and Technology (INP), a member of the Leibniz Health Research Alliance, Felix-Hausdorff-Str. 2, Greifswald 17489, Germany; Department of Dermatology and Venereology, University Medical Center Rostock, Strempelstr. 13, Rostock 18057, Germany. Electronic address: sander.bekeschus@med.uni-rostock.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionDiabetes mellitus is a chronic disease that can disrupt physiologic wound healing. Medical gas plasma technology produces therapeutic reactive species that support wound healing.

objectivePrevious studies have shown that increasing the transcriptional activity of the redox regulator nuclear factor erythroid 2-related factor 2 (Nrf2) in diabetic models can improve insulin sensitivity, reduce blood glucose levels, and ameliorate diabetic complications. However, the therapeutic potential and mechanisms of action of gas plasma have not been addressed in this context.

methodsFull-thickness dermal ear wounds were created in a preclinical mouse model of type II diabetes and compared with a native wild-type strain of C57BL/6 mice. First, the formation of reactive species in the plasma gas phase was determined by optical emission spectroscopy. Second, qPCR, protein expression, and inflammation analysis by cytokine secretion were performed to confirm the transcriptional results. Finally, qPCR and cytokine profiling were conducted to measure the effects of gas plasma in patient wound samples.

resultsRepeated in vivo treatment with medical gas plasma supported wound healing, e.g., re-epithelialization, in both sexes. Gas plasma-stimulated changes in Nrf2 signaling associated with downstream targets were supported by the evidence of impaired wound healing in Nrf2 knockout mice. In addition, gas plasma treatment significantly affected inflammation by modulating local and systemic cytokine levels. In vivo, treatment of human diabetic wounds underscored the involvement of Nrf2 signaling in protecting against oxidative stress, as assessed by qPCR. The cytokine signature of human diabetic wounds outlined different response patterns among patients after a single exposure, while inflammatory mediators were consistently reduced after repeated plasma treatment.

conclusionsThe present finding of accelerated wound healing by the Nrf2 activator underlines the high potential of medical gas plasma therapy in non-diabetic and diabetic wound healing.

Indexed as

Diabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2NF-E2-Related Factor 2Plasma GasesWound HealingAnimalsDisease Models, AnimalFemaleHumansMaleMiceMice, Inbred C57BLSignal TransductionNfe2l2 protein, mouseNF-E2-Related Factor 2Plasma GasesCytokinesDiabetes mellitusNrf2Plasma medicineReactive speciesRedox regulation

Identifiers

PMID40250557
PMCPMC12869232

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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.