Prdx2, a characteristic 2-Cys enzyme, is one of the most effective scavenger proteins against reactive oxygen species (ROS) and hydrogen peroxide (H2O2), protecting cells from oxidative stress. It is involved in multiple signaling pathways and plays a crucial role in maintaining cellular redox balance. Dysregulation of Prdx2 can lead to increased ROS levels and oxidative stress, which are implicated in various diseases [2].

In a study on non-alcoholic steatohepatitis (NASH), liver-specific Prdx2 knockout (Prdx2 LKO) female mice fed a methionine-choline deficient diet (MCD) showed a significant increase in hepatic lipid accumulation, inflammation, circulating aspartate aminotransferase (AST) levels, and activation of pro-inflammatory signaling pathways. There was also an increase in lipid peroxidation in the liver, suggesting that Prdx2 deficiency exacerbates MCD-induced NASH in female mice and indicating a protective role of Prdx2 [3]. In another study, endothelial-specific overexpression of Prdx2 improved cardiac microvascular function in a manner similar to isorhapontigenin treatment, and Prdx2 mediated the inhibition of ferroptosis by suppressing oxidative stress, iron overload, and lipid peroxidation [1].

In conclusion, Prdx2 is essential for maintaining cellular redox balance and has a protective role in various disease conditions. The use of Prdx2 knockout mouse models has provided valuable insights into its role in diseases such as NASH and cardiac microvascular injury, highlighting its potential as a therapeutic target for these diseases.