Table 2.

Summary of the promising mechanisms of ischemia reperfusion injury minimization currently being used in in vivo and in vitro models.

	Current Model	Intervention	Results
Complement Regulation	Pig-to-NHP in vivo transplant	Porcine transgenesis of human complement regulatory proteins such as hCD46	Successful transgenic pig to NHP xenotransplantation (Heart, Kidney, Lung)
Coagulation Regulation	Pig-to-NHP in vivo transplant	Porcine transgenesis of coagulation regulatory proteins such as hTBM, hTFPI, hEPCR	Successful transgenic pig to NHP xenotransplantation (Heart, Kidney, Lung)
Anti-inflammatory Medications	Pig-to-NHP in vivo transplant	Anti-IL1, Anti-IL6R, Anti-TNFα	Successful transgenic pig to NHP xenotransplantation (Heart, Kidney, Lung)
Ex vivo Cold perfusion	Pig-to-NHP in vivo transplant	Cold continuous ex-vivo reperfusion followed by intermittent reperfusion during organ implant until cross clamp is removed	Successful transgenic pig to NHP xenotransplantation with long term heart xenograft survival
Self-recognition proteins	Pig-to-NHP in vivo transplant	Porcine transgenesis of self-recognition proteins such as hCD47, hHLA-E	Successful transgenic pig to NHP xenotransplantation (Heart, Kidney, Lung)
Mesenchymal Stromal Cells (MSCs)	Human-to-sheep myocardial infarction (MI) Human-to-Canine cardiopulmonary bypass (CPB)	Intracoronary injection of MSCs Intravenous injection of MSCs	MI model – improved myocardial perfusion in the treated group CPB model – decreased inflammatory cytokine levels
Heme-oxygenase-1	Pig-to-human in vitro oxidative stress model	Porcine transgenesis of HO-1 put under oxidative stress and by human TNF in in vitro conditions	Reduced reactivity to oxidative and human TNF.