Oxeiptosis: a discreet way to respond to radicals

One of the best-studied cellular responses to toxic signals and pathogens is programmed cell death. Over the past years, it became apparent that the specific mechanisms of cell death have tremendous influence at both cellular and organismal level, highlighting the importance of sensors and pathways involved in this decision-making process. Central signalling molecules involved in a variety of cell death pathways are reactive oxygen species (ROS). However, the molecular mechanisms regulating differential responses and cellular fates to distinct ROS levels remain incompletely understood. Recently, we uncovered a caspase-independent cell-death pathway named ‘oxeiptosis’, which links the ROS sensing capacity of KEAP1 to a cell death pathway involving PGAM5 and AIFM1. Alike apoptosis, oxeiptosis is anti-inflammatory when activated by increased intracellular ROS levels and upon pathogens encounter. Here we discuss the potential impact of oxeiptosis in pathogens clearance and teratogenic cells.