Redox regulation meets metabolism: targeting PRDX2 to prevent hepatocellular carcinoma

Metabolic dysfunction-associated steatohepatitis (MASH) is emerging as a major driver of hepatocellular carcinoma (HCC). Crouchet et al. identify PRDX2 as a key regulator linking oxidative stress, metabolic imbalance, and oncogenic signaling. Across multiple in vivo and in vitro models, PRDX2 inhibition restores metabolic homeostasis, reduces tumor initiation, and selectively impairs HCC cell survival. These findings highlight PRDX2 as a promising biomarker and hepatocyte-directed target for chemoprevention, emphasizing the importance of the interplay between metabolism and liver cancer development.