Glutathione Peroxidase 4 (GPX4)

Where the papers sit

18 papers from the last 6 months study Glutathione Peroxidase 4 (GPX4) directly · updated from PubMed 12 Oct 2026

• Ferroptosis in Cancer and Tissue Injury

  Ferroptosis is being positioned as a way to kill cancer cells by weakening GPX4-dependent redox defense and increasing lipid peroxidation. HCC work links MRPS30-mediated GPX4 suppression to tumor progression, while curcumin and RSL3 provide induction strategies. Iron nanocomposites and membrane-mimetic platforms add photothermal or immunotherapy synergy. The same biology also frames platinum sensitivity in ovarian cancer and protection from cisplatin kidney injury, creating a therapeutic balance between inducing and blocking ferroptosis.

  7 papers · 38.9%

• GPX4 Ferroptosis Modulation

  GPX4 ferroptosis modulation is being applied in both cancer treatment and protection of vulnerable tissues. Lapatinib and arsenic trioxide are linked to ferroptosis through ATF4/GPX4 and USF1/GPX4, while MYC-driven FTH1/GPX4 suppression helps explain oxaliplatin resistance. RNAi lipid nanoparticles and engineered exosomes are used to deliver ferroptosis control more selectively. The direction is therefore bidirectional: induce ferroptosis in tumors, but restrain it in cardiomyocytes, diabetic tubules, and acute glaucoma.

  6 papers · 33.3%

• Therapeutic Ferroptosis Targeting

  Targeted ferroptosis is emerging as a therapeutic strategy in both cancer and inflammatory disease. In triple-negative breast cancer, DA-5 and sorafenib/miRNA delivery aim to disable GPX4 defenses and amplify lipid peroxidation. These approaches pair direct GPX4 inhibition with nanodelivery and immunoactivation rather than relying on nonspecific toxicity. A separate sepsis study shifts the goal, using irinotecan to inhibit FAR1 and restrain intestinal macrophage ferroptosis.

  3 papers · 16.7%

• NRF2 and GPX4 Redox Signaling

  NRF2–GPX4 redox signaling is being examined as a control point for ferroptosis under oxidative and inflammatory stress. In breast carcinoma, pyrazolone heterocycles promote ferroptosis by suppressing the NRF2/HMOX1/GPX4 axis. In hypoxic inflammatory pathology, neutrophil extracellular traps are linked to GPX4 downregulation and ferroptotic injury. The recurring therapeutic idea is to tune antioxidant defense, although the balance between tumor killing and tissue damage remains context dependent.

  2 papers · 11.1%