GPX4 regulates cellular necrosis and host resistance in Mycobacterium tuberculosis infection

• Published in: The Journal of experimental medicine Vol. 219; no. 11
• Main Authors: Amaral, Eduardo P, Foreman, Taylor W, Namasivayam, Sivaranjani, Hilligan, Kerry L, Kauffman, Keith D, Barbosa Bomfim, Caio Cesar, Costa, Diego L, Barreto-Duarte, Beatriz, Gurgel-Rocha, Clarissa, Santana, Monique Freire, Cordeiro-Santos, Marcelo, Du Bruyn, Elsa, Riou, Catherine, Aberman, Kate, Wilkinson, Robert John, Barber, Daniel L, Mayer-Barber, Katrin D, Andrade, Bruno B, Sher, Alan
• Format: Journal Article
• Language: English
• Published: United States Rockefeller University Press 07.11.2022
• Subjects: Animals; Ferroptosis; Glutathione - metabolism; Glutathione Peroxidase - metabolism; Infectious Disease and Host Defense; Innate Immunity and Inflammation; Lipid Peroxidation; Metabolism; Mice; Mice, Transgenic; Necrosis; Phospholipid Hydroperoxide Glutathione Peroxidase; Tuberculosis - immunology; Tuberculosis - metabolism

Cellular necrosis during Mycobacterium tuberculosis (Mtb) infection promotes both immunopathology and bacterial dissemination. Glutathione peroxidase-4 (Gpx4) is an enzyme that plays a critical role in preventing iron-dependent lipid peroxidation-mediated cell death (ferroptosis), a process previous...