ArticleCell death & disease2019
The classical NLRP3 inflammasome controls FADD unconventional secretion through microvesicle shedding.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 45 citations in OpenAlex.
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- Chemotherapy-induced activation of caspase-1 and IL-1α release by cancer cells remotely skews myelopoiesis to drive pro tumorigenic systemic neutrophil-dominant inflammation.Nature communications · 2026Article
- Exosome-Mediated Intercellular Communication in the Pathological Processes of Gouty Arthritis and Its Treatment.International journal of molecular sciences · 2026Review
- Role of BMEC-Derived Exosomal miR-144-3p in Microglial Polarization: Unveiling the NLRP3-GSDMD Pathway in Intracerebral Hemorrhage.Mediators of inflammation · 2026Article
- TGFβ1 attenuates microglial IL1β release through inhibition of NLRP3 inflammasome priming.Frontiers in immunology · 2025Article
- Evidence for a RIPK1-independent survival mechanism for CASPASE-8 in αβ T cells.Discovery immunology · 2025Article
- Naringenin can Inhibit the Pyroptosis of Osteoblasts by Activating the Nrf2/HO-1 Signaling Pathway and Alleviate the Differentiation Disorder of Osteoblasts Caused by Microgravity.Journal of agricultural and food chemistry · 2024Article
- Exposing kinetic disparities between inflammasome readouts using time-resolved analysis.Heliyon · 2024Article
- Inflammasome Molecular Insights in Autoimmune Diseases.Current issues in molecular biology · 2024Review
- Exosomes derived from programmed cell death: mechanism and biological significance.Cell communication and signaling : CCS · 2024Review
- Ibuprofen inhibits anaplastic thyroid cells in vivo and in vitro by triggering NLRP3-ASC-GSDMD-dependent pyroptosis.Inflammopharmacology · 2024Article
- Deciphering the therapeutic potential of trimetazidine in rheumatoid arthritisFrontiers in pharmacology · 2024Article
- Infrapatellar fat pad adipose tissue-derived macrophages display a predominant CD11c+CD206+ phenotype and express genotypes attributable to key features of OA pathogenesis.Frontiers in immunology · 2024Article
- Nanostructured Microparticles Repolarize Macrophages and Induce Cell Death in an In Vitro Model of Tumour-Associated Macrophages.Pharmaceutics · 2023Article
- Bioinformatic identification and validation of autophagy-related genes in rheumatoid arthritis.Clinical rheumatology · 2023Article
- Inflammasomes as biomarkers and therapeutic targets in traumatic brain injury and related-neurodegenerative diseases: A comprehensive overview.Neuroscience and biobehavioral reviews · 2023Review
- The regulatory role and therapeutic application of pyroptosis in musculoskeletal diseases.Cell death discovery · 2022Review
- Tanshinone IIA reduces pyroptosis in rats with coronary microembolization by inhibiting the TLR4/MyD88/NF-κB/NLRP3 pathway.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2022Article
- Fas/CD95 Signaling Pathway in Damage-Associated Molecular Pattern (DAMP)-Sensing Receptors.Cells · 2022Review
- Resting time after phorbol 12-myristate 13-acetate in THP-1 derived macrophages provides a non-biased model for the study of NLRP3 inflammasome.Frontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fas-associated death domain (FADD) is a key adaptor molecule involved in numerous physiological processes including cell death, proliferation, innate immunity and inflammation. Therefore, changes in FADD expression have dramatic cellular consequences. In mice and humans, FADD regulation can occur through protein secretion. However, the molecular mechanisms accounting for human FADD secretion were still unknown. Here we report that canonical, non-canonical, but not alternative, NLRP3 inflammasome activation in human monocytes/macrophages induced FADD secretion. NLRP3 inflammasome activation by the bacterial toxin nigericin led to the proinflammatory interleukin-1β (IL-1β) release and to the induction of cell death by pyroptosis. However, we showed that FADD secretion could occur in absence of increased IL-1β release and pyroptosis and, reciprocally, that IL-1β release and pyroptosis could occur in absence of FADD secretion. Especially, FADD, but not IL-1β, secretion following NLRP3 inflammasome activation required extracellular glucose. Thus, FADD secretion was an active process distinct from unspecific release of proteins during pyroptosis. This FADD secretion process required K
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.