Atypical Diabetic Foot Ulcer Keratinocyte Protein Signaling Correlates with Impaired Wound Healing

Figure 4

Schematic representation of the signaling dysregulation in DFUs compared to normal tissues and boxplots of those analytes significantly altered between the two tissues. (a) Simplified scheme of the dynamic Akt switch between DFU and normal tissues. Increased levels of PTEN-mediated, PI3 kinase-induced activation of Akt promote competing mechanisms of normal or impaired healing. (b) The calculated ratios for significantly modulated analyte/Akt ratios (boxplots) for DFU () and normal () study subjects representative of (1) normal apoptosis (Bak and Caspase-9) and increased angiogenesis (iNOS and VEGFR1) for the normal wound healing response (depicted in (a)) and (2) inhibition of survival (GSK-3β, β-Catenin, and NFκB) and activation of senescence (p53 and p16INK4a) for the impaired wound healing response (depicted in (a)). These groups may represent potential targets for the development of therapies for the treatment, or prevention, of DFU wounds.

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