ArticleScientific reports2023
Negative pressure wound therapy promotes wound healing of diabetic foot ulcers by up-regulating PRDX2 in wound margin tissue.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. It is linked to trial NCT07557524 (PULSED HIGH INTENSITY LASER VERSUS NEGATIVE PRESSURE THERAPY ON NEUROPATHIC ULCERS), which is not on this map. Cited by 12 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
Pulsed high intensity laser versus negative pressure therapy on neuropathic ulcers
Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.
- The Underlying Mechanisms and Role of Negative Pressure Wound Therapy in Chronic Diabetic Wound Healing: A Systematic Review and Meta-Analysis.International wound journal · 2026Pooled it
- Identification of characteristic genes of pressure ulcers based on angiogenesis-related genes and construction of miRNA, transcription factor, and molecular drug regulatory networks.BMC immunology · 2026Article
- Microfluidics, 3D bioprinted scaffold and organ-on-chip with biosensing activated therapeutic strategies for diabetic wound healing.Frontiers in bioengineering and biotechnology · 2026Review
- Immune cells in diabetic wound repair: the key to better wound management.Frontiers of medicine · 2025Review
- Temporal Regulation of Early-Stage Cytokine Expression in Diabetic Wound Healing Under Negative Pressure Wound Therapy.International journal of molecular sciences · 2025Article
- Ischemia/reperfusion-associated oxidative stress is an aggravating factor for pressure ulcers.Journal of clinical biochemistry and nutrition · 2025Article
- Acid-responsive CST@NPs enhanced diabetic wound healing through rescuing mitochondrial dysfunction.Bioactive materials · 2025Article
- NFAT5 exacerbates β-cell ferroptosis by suppressing the transcription of PRDX2 in obese type 2 diabetes mellitus.Cellular and molecular life sciences : CMLS · 2025Article
- A comprehensive review on diabetic foot ulcer addressing vascular insufficiency, impaired immune response, and delayed wound healing mechanisms.Frontiers in pharmacology · 2025Review
- Platelet-Rich Plasma in Diabetic Foot Ulcer Healing: Contemplating the Facts.International journal of molecular sciences · 2024Review
- Enhancing diabetic foot ulcer healing: Impact of the regulation of the FUS and ILF2 RNA‑binding proteins through negative pressure wound therapy.International journal of molecular medicine · 2024Article
- Identifying and Validating Extracellular Matrix-Related Gene CTSH in Diabetic Foot Ulcer Using Bioinformatics and Machine Learning.Journal of inflammation research · 2024Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To understand the changes in the peroxiredoxin-2 (PRDX2) expression level in the wound margin tissue (T-PRDX2) of patients with diabetic foot ulcer (DFU) before and after negative pressure wound therapy (NPWT). Additionally, the study aimed to explore the association between PRDX2 expression and the treatment outcome of DFUs to provide a new theoretical basis for revealing the mechanism of NPWT promoting the healing of DFUs. Fifty-six type 2 diabetes patients with foot ulcers undergoing NPWT (the DFU group) and 28 patients with chronic lower limb skin ulcers with normal glucose tolerance undergoing NPWT (the skin ulcer control [SUC] group) were included in the study. T-PRDX2 was detected using Western blotting, and the superoxide dismutase (SOD) activity and the malondialdehyde (MDA) and glutathione (GSH) levels were detected using a biochemical method. In addition, in vitro experiments were conducted to determine the effect of PRDX2 expression on normal human dermal fibroblast (NHDF) proliferation, migration, and apoptosis. Before NPWT, the DFU group exhibited a significantly lower T-PRDX2 expression level compared with the SUC group. After one week of NPWT, the T-PRDX2 expression level, SOD activity, and GSH content in the wound margin tissues of the DFU and SUC groups significantly increased compared with the before NPWT levels. Conversely, the inflammatory indicators (white blood cell, neutrophil percentage, C-reactive protein, and procalcitonin) and MDA content were significantly lower than the before NPWT levels. The expression changes of T-PRDX2 before and after NPWT in the DFU and SUC groups were positively correlated with the 4-week wound healing rate. In vitro experiments demonstrated that PRDX2 could alleviate the oxidative stress in NHDFs, thereby promoting their proliferation and migration, while reducing cell apoptosis. NPWT promotes DFU healing by increasing T-PRDX2, and changes in the T-PRDX2 might be associated with the therapeutic effect of NPWT.
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