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Observations that rats treated with CsA develop hypertension prior to myocardial hypertrophy (101, 153155) supported the notion that perhaps the clinical hypertrophic phenotype is purely related to CNI-induced hypertension rather than direct myocardial effects

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The continuous production of ONOO could suppress the activity of glutathione reductase by nitration modification, thus collectively reducing detoxification and blocking DNA damage repair

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