Prdx1, short for peroxiredoxin 1, is a member of the peroxidase family. It functions mainly in protecting cells against damage caused by H2O2 and also acts as a molecular chaperone in various biological processes. Prdx1 is involved in multiple pathways such as TLR4-NFκB signaling, autophagy, and redox-regulation, which are crucial for maintaining cellular homeostasis and are related to many disease-related processes [2].

In a study using PRDX1-knockdown (PRDX1KD) cells, it was found that PRDX1 negatively regulates TLR4 signaling for NFκB activation and autophagy functions. PRDX1KD THP-1 cells showed increased NFκB activation, pro-inflammatory cytokine production, and resistance against Salmonella typhimurium infection. Also, the migration and invasion abilities of PRDX1KD cancer cells were enhanced, indicating its role in cancer-related processes [1]. In PRDX1 knockout mice, the number of AOM/DSS-induced colitis-associated CRC was significantly lower, accompanied by downregulation of NRF2 and GPX4. Mechanistically, PRDX1 knockdown led to ROS-induced mitochondrial dysfunction and lipid peroxidation-induced ferroptosis in CRC cells [3].

In conclusion, Prdx1 plays essential roles in maintaining cellular redox balance, regulating autophagy, and influencing cancer-related processes. Gene knockout models, especially in mice, have provided significant insights into its functions in diseases like cancer and inflammatory bowel diseases, helping to understand the underlying mechanisms and potentially paving the way for new therapeutic strategies targeting Prdx1.