Nuclear factor erythroid 2-related factor 2 (NRF2)

Where the papers sit

50 papers from the last 6 months study Nuclear factor erythroid 2-related factor 2 (NRF2) directly · updated from PubMed 10 Oct 2026

• KEAP1-NRF2 Therapeutics

  Therapeutic activation of NRF2 is moving from broad antioxidant approaches toward direct disruption of the KEAP1-NRF2 interaction. Candidate treatments address diabetic kidney and wound disease, neurotoxicity, lung injury, ferroptosis and inflammatory tissue damage. Natural products and engineered delivery systems repeatedly converge on NRF2, HO-1, NLRP3 and iron-handling pathways, while GSK3227634 represents a more selective pharmacologic strategy. Most evidence remains preclinical, with tissue targeting, durability and safety still open questions.

  18 papers · 36%

• Oxidative Stress and Ferroptosis

  NRF2 modulation is being used either to prevent oxidative and ferroptotic tissue damage or, in cancer, to intensify lethal ROS accumulation. HO-1, SLC7A11 and GPX4 recur as the main control points linking redox balance to ferroptosis. Protective studies span neural, retinal, renal, skin and spinal injury, whereas hepatocellular and breast cancer studies pursue selective oxidative collapse. The opposing therapeutic aims make disease context and pathway direction decisive.

  16 papers · 32%

• Ferroptosis and Mitochondrial Stress

  NRF2-linked control of ferroptosis is being examined as a route to protect organs from dietary, metabolic and toxic injury. The recurring mechanism involves HO-1, GPX4, iron handling and lipid peroxidation, often alongside mitochondrial dysfunction and inflammation. Natural compounds, drug candidates and delivery systems generally aim to restore redox balance rather than target ferroptosis alone. Evidence remains largely preclinical and spans kidney, brain, vasculature, retina and reproductive tissues.

  12 papers · 24%

• Liver Lipid Metabolism

  Metabolic dysfunction-associated steatotic liver disease is being linked to hepatic cholesterol sensing, lipoprotein export and redox-regulated metabolism. The NFE2L1-INSIG1 interaction emerges as a control point for VLDL secretion and steatohepatitis pathogenesis. Other work adds m6A and compensatory arginine methylation as possible routes from metabolic dysfunction to premalignant change. Aging, sex and NRF2 status remain important modifiers of the gut-metabolism and liver-disease axis.

  4 papers · 8%