ArticleAmerican journal of translational research2020
PKCβ increases ROS levels leading to vascular endothelial injury in diabetic foot ulcers.
Article in American journal of translational research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The trial behind it
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Who cites it
9 citing papers in PubMed, 8 citations in OpenAlex.
- Negative pressure wound therapy (NPWT) is superior to conventional moist dressings in wound bed preparation for diabetic foot ulcers: A randomized controlled trial.Saudi medical journal · 2023Trial
- SETD2 Improves Endothelial Function and Angiogenesis in Diabetic Hindlimb Ischemia Via Activating ANGPT2-PI3K/AKT Pathway.Cardiovascular toxicology · 2026Article
- Abnormally Elevated PKCδ Delays Diabetic Wound Healing by Inhibiting the GAD1-GABA Pathway.Diabetes & metabolism journal · 2026Article
- Circular RNAs in Diabetic Foot Ulcers: A Scoping Review of Clinical, Preclinical, and In Silico Evidence on Diagnostic and Therapeutic Potentials.Endocrinology, diabetes & metabolism · 2026Article
- Role of nuclear factor erythroid 2-related factor 2 in negative pressure wound therapy for diabetic foot ulcers.World journal of diabetes · 2025Article
- Mesenchymal Stem Cell-Derived Exosomes Hold Promise in the Treatment of Diabetic Foot Ulcers.International journal of nanomedicine · 2025Review
- The role of oxidative stress in diabetes mellitus-induced vascular endothelial dysfunction.Cardiovascular diabetology · 2023Review
- Hyperbaric Oxygen Therapy Reduces Oxidative Stress and Inflammation, and Increases Growth Factors Favouring the Healing Process of Diabetic Wounds.International journal of molecular sciences · 2023Article
- Curcumin coated 3D biocomposite scaffolds based on chitosan and cellulose for diabetic wound healing.Heliyon · 2022Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo explore the role and mechanism of oxidative stress injury in the diabetic foot.
methodsImmunohistochemistry and staining were used to detect changes in diabetic foot tissue, and the CCK-8 method was used to measure high glucose effect on cell viability. The DCFH-DA assay was used to detect the intracellular ROS content, and colorimetric methods were used to detect the activities of the CAT and SOD enzymes and the NO and MDA content in tissues and cells. In addition, the protein expression levels of PKCβ, p66shc, eNOS, ICAM-1 and NF-κB in tissues and cells were detected by Western blotting, and the distribution of p66shc and eNOS was observed by immunofluorescence.
resultsThe results of clinical specimens experiments showed that the DFU group exhibited disordered morphology and increased glucose metabolism, decreased activities of the enzymes CAT and SOD in tissues, and increased MDA and NO contents compared to those in the CON group. Furthermore, protein levels of the p-PKCβ, p-p66shc, ICAM-1, and p-NF-κB were increased, and eNOS protein level was decreased; these results were consistent in clinical specimens and in vitro experiments.
conclusionsHigh glucose levels may induce oxidative stress injury in cells and tissues by activating the PKCβ-p66shc signaling pathway.
Indexed as
Identifiers
33194039PMC7653566W3103916319What OpenQuestion holds
Registered trials
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.