Ischemia–reperfusion injury is characterized by a sublethal injury to epithelial cells resulting in the release of TLR activating danger signals. These danger signals promote the production of chemokines, cytokines, oxygen free radicals and the extravasation of leucocytes from the circulation that amplifies cell damage. Compounds which block TLR activation represent a novel therapeutic mechanism to inhibit this pro-inflammatory cascade thus reducing I/R damage and improving organ function.
