Abstract
Diabetic foot ulcers (DFUs) are a severe complication of diabetes and a common cause of lower limb amputations and are associated with a high mortality rate. We previously demonstrated that the transcription factor SOX2 establishes a transcriptional network that primes the oral epithelium for rapid wound repair and reprogrammed cutaneous keratinocytes to present accelerated wound resolution both in vitro and in vivo. However, the mechanisms by which SOX2 reverses effects of diabetes during wound healing are not known.
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