TGFB1 and neuroblastoma: 2021). In UUO, high levels of NOX induced the overproduction of mitochondrial ROS generation which promotes oxidative stress. ROS overproduction by NOXs and mitochondria activates TGF-β1, which is a crucial mediator in promoting fibrosis. PCA treatment was able to prevent this cascade by improving mitochondrial function and inhibiting ROS production in human neuroblastoma cell line SH-SY5Y cells (Guo et al. 2019). PCA treatment also suppresses cisplatin-induced injury in vitro by blocking NOX-mediated oxidative stress (Gao et al. 2016).