Although emerging evidences have shown that miR-203 participates in the development of diabetic nephropathy by targeting regulating the expression of semaphorin 3A, resultingly inhibiting oxidative stress, or that it participates in the pathogenesis of diabetic cardiomyopathy by regulating the expression of PI3KCA, thereby inhibiting oxidative stress [23], as far as we know, no investigations have been performed on the molecular mechanism of miR-203 in CI/R oxidative stress injury. This evidence concerns the gene SEMA3A and diabetic cardiomyopathy.