Moreover, MI-induced accumulation of mitochondrial ROS was associated with cardiac fibroblasts activation [23], suggesting that cardiac fibroblasts are potential cellular targets for antioxidant therapies in HF. Notably, the present studies reported that Ala could substantially protect against organ fibrosis via inhibiting the production of ROS in pressure overload-induced cardiomyocytes, AngII-induced hepatocytes, and I/R-induced NRK52E cells [17, 24, 25]. Here, AGT is linked to hydrops fetalis.