Ischemia reperfusion injury (IRI) contributes to inflammation, acute rejection, and negatively impacts VCA function and survival. Strategies to prevent IRI could decrease rejection episodes, improve VCA outcomes and facilitate immune tolerance induction strategies. Galectin-3 (Gal3), a beta-galactoside binding lectin, contributes to acute inflammation in response to tissue hypoxia, an unavoidable consequence of organ harvest and VCA transplantation. Blocking extracellular Gal3 using known Gal3 inhibitors including modified citrus pectin (MCP) has been shown in animal models to reduce inflammation and fibrosis. This proposal will elucidate the role of Gal3 in VCA IRI. We hypothesize that Gal3 significantly contributes to VCA IRI and that blocking extracellular Gal3 function using MCP can serve as a novel therapeutic approach to prevent or reduce IRI. We also hypothesize that circulating Gal3 levels can serve as a predictive biomarker of IRI and VCA function post transplantation.