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Likewise, hearts of IGF-1 transgenic mice were protected from ischemia and reperfusion [83], and streptozotocin-induced diabetic cardiomyopathy in mice resulted in accumulation of nitrotyrosine (a reactive oxygen product) in vivo and the formation of H 2 O 2 in myocytes in vitro that were rescued in IGF-1 transgenic mice [84]
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