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Oxeiptosis, a ROS-induced caspase-independent apoptosis-like cell-death pathway.
Nat. Immunol. 19, 130–140 (2017)
Reactive oxygen species (ROS) are generated by virus-infected cells; however, the physiological importance of ROS generated under these conditions is unclear. Here we found that the inflammation and cell death induced by exposure of mice or cells to sources of ROS were not altered in the absence of canonical ROS-sensing pathways or known cell-death pathways. ROS-induced cell-death signaling involved interactions among the cellular ROS sensor and antioxidant factor KEAP1, the phosphatase PGAM5 and the proapoptotic factor AIFM1. Pgam5(-/-) mice showed exacerbated lung inflammation and proinflammatory cytokines in an ozone-exposure model. Similarly, challenge with influenza A virus led to increased infiltration of the virus, lymphocytic bronchiolitis and reduced survival of Pgam5(-/-) mice. This pathway, which we have called 'oxeiptosis', was a ROS-sensitive, caspase independent, non-inflammatory cell-death pathway and was important for protection against inflammation induced by ROS or ROS-generating agents such as viral pathogens.
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Publikationstyp
Artikel: Journalartikel
Dokumenttyp
Wissenschaftlicher Artikel
Schlagwörter
Oxidative Stress; Nadph Oxidase; Molecular-mechanisms; Hydrogen-peroxide; Virus; Keap1; Protein; Necroptosis; Activation; Nrf2
ISSN (print) / ISBN
1529-2908
e-ISSN
1529-2916
Zeitschrift
Nature Immunology
Quellenangaben
Band: 19,
Heft: 2,
Seiten: 130–140
Verlag
Nature Publishing Group
Verlagsort
New York
Nichtpatentliteratur
Publikationen
Begutachtungsstatus
Peer reviewed
Institut(e)
Institute of Diabetes and Obesity (IDO)