Signaling by ROS drives inflammasome activation

By Fabio Martinon. European Journal of Immunology, 2010

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Mitochondrial cardiolipin is required for Nlrp3 inflammasome activation (2013, background): “Linezolid-Induced Nlrp3 Inflammasome Activation Is Independent of ROS but Inhibited by Mitochondrial Stabilization with Cyclosporine A ROS generation has been suggested to be an absolute requirement for activation of the Nlrp3 inflammasome (Dostert et al., 2008; Martinon, 2010; Tschopp and Schroder,”
Redox Regulation of NLRP3 Inflammasomes: ROS as Trigger or Effector? (2015, neutral): “Being tightly regulated under normal conditions, intracellular and extracellular ROS are maintained at very low levels, which play physiological signaling roles (less than 1% of produced ROS) (41, 61, 77, 108, 138).”
Combating oxidative stress in vascular disease: NADPH oxidases as therapeutic targets (2011, background): “Moreover, it was recently suggested that ROS initiate the assembly of multiprotein signalling complexes known as inflammasomes , which activate caspase 1, and thereby lead to the processing and secretion of the pro-inflammatory cytokines interleukin-1β (IL-1β) and IL-18 (Ref”
The inflammasome: an integrated view (2011, background): “induced inflammasome activation (7, 60, 61, 96, 101), as many inflammasome activators induce ROS production by this complex.”