New Insights into Shear Stress–Driven NRF2 Dysfunction in Venous Disease

In a recent publication in Biomedicine & Pharmacotherapy, Dr Sumi and her group investigate the role of NRF2-mediated antioxidant signaling in vascular endothelial dysfunction under pathological shear stress conditions. The study titled, “Flow-dependent NRF2 dysfunction via KEAP1/WDR23 dual repression contributes to endothelial oxidative damage in venous disease”, reveals how altered hemodynamic forces disrupt endothelial redox balance through mechanosensitive regulation of the NRF2 pathway, leading to increased oxidative stress and vascular injury. Using human varicose vein tissue samples and advanced in vitro flow models, the research provides mechanistic insights into the interplay between shear stress, oxidative signaling, and endothelial integrity.

The findings highlight the therapeutic potential of targeting NRF2-associated pathways to mitigate oxidative damage in chronic venous diseases and advance redox-mechanobiology-based treatment strategies.