Reoxygenation of ischemic tissue is essential for survival. Paradoxically, however, it can increase the damage produced by hypoxia, which is known as ischemia-reperfusion (IR) injury. This type of damage underlies several pathologies, notably heart attack and stroke, and is caused, in part, by excessive reactive oxygen species production and mitochondrial dysfunction. Our aim is to determine the potential cardioprotective role of the transcription factor Nrf2 (nuclear factor erythroid 2-related factor 2) against IR injury. Nrf2 is a key regulator of the cellular redox balance and also of intermediary metabolism and mitochondrial function. We are also interested in the therapeutic potential of Nrf2 in doxorubicin-induced cardiotoxicity. For these studies we use cardiac cell lines and isolated perfused hearts (Langendorff) from mice lacking Nrf2 and a variety of experimental approaches and techniques.