NLRP3 inflammasome activation: the convergence of multiple signalling pathways on ROS production?
By J. Tschopp, Kate Schroder. Nature reviews. Immunology, 2010
1,858 citations recorded by the source corpus.
Subfields: Molecular Biology, Pediatrics, Perinatology and Child Health
View Paper: https://www.semanticscholar.org/paper/22ebeb83c6e610bfda71e4d1fb63f4ec45811442
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In Molecular Biology
In Pediatrics, Perinatology and Child Health
Citations in the corpus
- Role of pyroptosis in inflammation and cancer (2022, background): “Upon stimulation with hypoxia, Neat1 will facilitate the activation of the NLRP3 inflammasome and directly interact with the caspase-1 p20 subunit through its 5’ end, and it can combine with procaspase-1 to stabilize the aggregation of the complex or with the mature caspase-1 tetramer to increase it”
- Redox Regulation of NLRP3 Inflammasomes: ROS as Trigger or Effector? (2015, positive): “For example, excessive levels of ATP were described as one of the first endogenous DAMPs to induce NLRP3 inflammasome formation and activation, a mechanism involving high concentrations of extracellular ATP binding to the purinergic P2X7 receptor (104).”
- Intratumor T helper type 2 cell infiltrate correlates with cancer-associated fibroblast thymic stromal lymphopoietin production and reduced survival in pancreatic cancer (2011, background): “Endogenous factors released by dead and dying tumor cells or present in the tumor microenvironment might serve as endogenous stimuli for NF-kB and inflammasome activation required for proinflammatory cytokine activation and release (Tschopp and Schroder, 2010; Fig.”
- Inflammasomes and their roles in health and disease. (2012, background): “…tularensis dampens AIM2 inflammasome-mediated IL-1β secretion and macrophage pyroptosis with its putative lipid II flippase mviN, whereas Mycobacterium tuberculosis inhibits activation of the Nlrp3 inflammasome using the putative Zn2+ metalloprotease zmp1 (Master et al. 2008, Ulland et al. 2010).”
- Oxidized mitochondrial DNA activates the NLRP3 inflammasome during apoptosis. (2012, neutral): “In the past, three models of NLRP3 activation were proposed: reactive oxygen species (ROS) generation (Tschopp and Schroder, 2010), lysosomal damage (Hornung and Latz, 2010), and cytosolic K+ efflux (Pétrilli et al., 2007).”
- The role of oxidative stress during inflammatory processes (2013, background): “The third model, termed the ROS model (Tschopp and Schroder, 2010), implicates the formation of ROS, deregulation of cellular redox status, and mitochondrial stress as key mechanisms in the process of NLRP3 activation (Rubartelli et al., 2011; Zhou et al., 2011; Rubartelli, 2012).”
- NLRP3 inflammasome: From a danger signal sensor to a regulatory node of oxidative stress and inflammatory diseases (2015, neutral): “…. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 302 References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 304”
- Cholesterol Crystals Activate the NLRP3 Inflammasome in Human Macrophages: A Novel Link between Cholesterol Metabolism and Inflammation (2010, background): “Potassium efflux [32], leakage of lysosomal cathepsin B into the cytoplasm [24], and/or reactive oxygen species formation [14] caused by these substances seem to be essential intermediate steps in activation of NLRP3 receptor, although the interplay between these processes is poorly understood [11,1”
- Role of nrf2 in oxidative stress and toxicity. (2013, background): “The inflammasomes are a molecular platform required for fully functional innate immune systems (102).”