Excessive reactive oxygen species (ROS) formation and mitochondrial dysfunction are common denominators in several cardiovascular diseases; thus, identifying and pharmacologically targeting ROS sources may prove as an efficient way to protect diseased hearts. In this video, Dr. Kaludercic reviews the role of monoamine oxidase (MAO)-dependent ROS formation and mitochondrial dysfunction in heart failure, diabetic cardiomyopathy and doxorubicin-induced cardiotoxicity. Moreover, she highlights some of the ongoing work showing that ROS produced by MAO also play a physiological role and are important for cardiomyocyte differentiation.

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