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Overexpression of human copper/zinc superoxide dismutase (SOD1) suppresses ischemia-reperfusion injury and subsequent development of graft coronary artery disease in murine cardiac grafts.
Early inhibition of caspase-3 activity lessens the development of graft coronary artery disease.
Caspase-3 inhibition preserves myocardial geometry and long-term function after infarction.