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The increasing number of diabetes patients represents a health challenge due to disease-related, end-organs complications. Hyperglycemia is considered the proximal trigger of an intricate cascade of molecular processes that progressively deteriorate tissues and organs, leading to the onset of clinical complications. Lower extremity ulcerations and their ensued refractoriness to heal can potentially result in amputation and disability and remain the second most feared diabetic complication. We have identified particular morphogenetic traits in diabetic foot ulcer granulation tissues and its cultured fibroblasts. Diabetic ulcerderived fibroblasts conserve a sort of memory as their in vitro traits very much recapitulate the in vivo behavior, in terms of proliferative disabilities and transcriptional and post-translational modifications of genes involved in proliferation, migration and ECM dinamics. Furthermore, the acute, in vivo morphologic recreation of a microangiopathy in a neo-formed granulation tissue is worth mentioning. All these elements suggest that “metabolic memory,” in which chromatin remodeling and long-lasting epigenetic changes play important roles, could contribute to the persistence of diabetic complications. Metabolic memory is largely responsible for the onset/perpetuation of the ulcers chronicity phenotype . The comprehensive understanding of the chromatin choreography underlying this pathogenic stream; and its potential pharmacologic manipulation would allow for future innovative therapies for diabetic complications, including wound healing refractoriness.

Torpid Diabetic Wound Healing: Evidence on the Role of Epigenetic Forces