Lipid Peroxidation-Dependent Cell Death Regulated by GPx4 and Ferroptosis.
By H. Imai, Masaki Matsuoka, T. Kumagai, Taro Sakamoto, Tomoko Koumura. Current Topics in Microbiology and Immunology, 2017
598 citations recorded by the source corpus.
Subfields: Cancer Research, Pharmacology, Pulmonary and Respiratory Medicine
View Paper: https://www.semanticscholar.org/paper/19d512af5623f8ad8969c33d2ac700022286834a
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In Cancer Research
In Pulmonary and Respiratory Medicine
Citations in the corpus
- Ferroptosis, necroptosis, and pyroptosis in anticancer immunity (2020, background): “Glutathione peroxidase 4 (GPX4), a selenoprotein harboring a selenocysteine (Sec) in its catalytic center, is required for an efficient reduction in peroxidized phospholipids [61, 62].”
- Mitochondria-dependent ferroptosis plays a pivotal role in doxorubicin cardiotoxicity (2020, unknown): “Gpx4 is a unique gene that encodes cytosolic, mitochondrial, and nucleolar isoforms (14).”
- Emerging mechanisms and disease relevance of ferroptosis (2020, background): “5 days post conception (dpc), conditional-Gpx4-mutant mice revealed that GPX4 loss not only induces ferroptosis, but also results in neurodegeneration [19], loss of antiviral immunity [61], infertility, and ischemia/reperfusion injury in kidney and liver [27,28,62,63].”