Abstract
Background: In addition to vasculopathy and poor wound healing, ischemia-reperfusion injury (IRI) is increasingly recognized as a factor that contributes to complications such as chronic wounds in diabetic patients. Recent work in our lab and others has shown that the endogenous signaling molecule hydrogen sulfide (HS) can mitigate IRI in a number of euglycemic animal models. However, in the setting of diabetes, in which tissues are known to be even more sensitive to the deleterious effects of IRI, there is a paucity of data regarding the cytoprotective effects of HS.
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