ArticleBioscience reports2018
Specific PKC βII inhibitor: one stone two birds in the treatment of diabetic foot ulcers.
Article in Bioscience reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 23 papers.
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.
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Who cites it
23 citing papers in PubMed, 34 citations in OpenAlex.
- Metabolic reprogramming in diabetic panvascular disease: Molecular mechanism and therapeutic strategies.iScience · 2026Review
- Multi-Omics Profiling Reveals Neutrophil Extracellular Trap Dysregulation in Diabetic Foot Ulcer Healing Impairment.International journal of molecular sciences · 2026Article
- Abnormally Elevated PKCδ Delays Diabetic Wound Healing by Inhibiting the GAD1-GABA Pathway.Diabetes & metabolism journal · 2026Article
- Neutrophils and neutrophil extracellular traps in diabetes mellitus and its complications: Mechanisms and therapeutic implications.iScience · 2026Review
- Investigating the Wound Healing Potential of CuCOBiological trace element research · 2026Article
- Neutrophil extracellular traps in diabetic wound healing: mechanisms, pathological roles, and therapeutic implications.Burns & trauma · 2026Review
- RETRACTION: Molecular Changes in Diabetic Wound Healing following Administration of Vitamin D and Ginger Supplements: Biochemical and Molecular Experimental Study.Evidence-based complementary and alternative medicine : eCAM · 2026Article
- Neutrophil Extracellular Traps in Diabetic Kidney Disease: Mechanisms of Pathogenesis and Emerging Therapeutic Strategies.Drug design, development and therapy · 2026Review
- Neutrophil Extracellular Traps in Wound Healing of Diabetes: Mechanisms, Inducers, and Therapeutic Implications.Mediators of inflammation · 2026Review
- Madecassoside mitigates acute myocardial infarction injury by activating the PKCB/SPARC signaling pathway.Acta pharmacologica Sinica · 2025Article
- Nonlinear association between atherogenic index of plasma and type 2 diabetes mellitus in overweight and obesity patients: evidence from Chinese medical examination data.Cardiovascular diabetology · 2024Article
- Neutrophils extracellular traps and ferroptosis in diabetic wounds.International wound journal · 2023Review
- Diabetic vascular diseases: molecular mechanisms and therapeutic strategies.Signal transduction and targeted therapy · 2023Review
- Excessive neutrophil extracellular trap formation induced byFrontiers in cellular and infection microbiology · 2023Article
- Diabetes-associated neutrophil NETosis: pathogenesis and interventional target of diabetic complications.Frontiers in endocrinology · 2023Review
- Neutrophil Extracellular Traps Delay Diabetic Wound Healing by Inducing Endothelial-to-Mesenchymal Transition via the Hippo pathway.International journal of biological sciences · 2023Article
- Investigation of Neutrophil Extracellular Traps as Potential Mediators in the Pathogenesis of Non-Acute Subdural Hematomas: A Pilot Study.Diagnostics (Basel, Switzerland) · 2022Article
- Regulation of endothelial progenitor cell functions during hyperglycemia: new therapeutic targets in diabetic wound healing.Journal of molecular medicine (Berlin, Germany) · 2022Review
- Enhanced neutrophil extracellular trap formation in COVID-19 is inhibited by the protein kinase C inhibitor ruboxistaurin.ERJ open research · 2022Article
- Emerging role of neutrophil extracellular traps in the complications of diabetes mellitus.Frontiers in medicine · 2022Review
Corrections and comments
- Retracted
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To explore whether or not inhibition of protein kinase C βII (PKC βII) stimulates angiogenesis as well as prevents excessive NETosis in diabetics thus accelerating wound healing. Streptozotocin (STZ, 60 mg/kg/day for 5 days, i.p.) was injected to induce type I diabetes in male ICR mice. Mice were treated with ruboxistaurin (30 mg/kg/day, orally) for 14 consecutive days. Wound closure was evaluated by wound area and number of CD31-stained capillaries. Peripheral blood flow cytometry was done to evaluate number of circulating endothelial progenitor cells (EPCs). NETosis assay and wound tissue immunofluorescence imaging were done to evaluate the percentage of neutrophils undergoing NETosis. Furthermore, the expression of PKC βII, protein kinase B (Akt), endothelial nitric oxide synthase (eNOS), vascular endothelial growth factor (VEGF), and histone citrullation (H3Cit) were determined in the wound by Western blot analysis. Ruboxistaurin accelerated wound closure and stimulated angiogenesis in diabetic mice. The number of circulating EPCs was increased significantly in ruboxistaurin-treated diabetic mice. Moreover, ruboxistaurin treatment significantly decreases the percentages of H3Cit
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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.