PRKN and Parkinson disease: In vitro studies corroborated this concept, i.e., overexpression of Parkin in isolated cardiomyocytes subjected to hypoxia-mediated cell death was associated with increased Parkin translocation to the mitochondria and increased cell viability, while cardiomyocytes expressing Parkinson disease-associated mutants of Parkin failed to reduce hypoxia-mediated cell death [204].