AGT and hydrops fetalis: Importantly, while the decrease in cytosolic ROS can be explained by a reduced O2•− release from NOXs, the reduced levels of mitochondrial ROS hint towards an interplay of NOX activation and mitochondrial ROS production in CMs in our setting of EtOH induced HF/ACA-overload, a mechanism that has been described in angiotensin II-induced oxidative stress29, 30.