ArticleEMBO reports2022
GM-CSF suppresses antioxidant signaling and drives IL-1β secretion through NRF2 downregulation.
Article in EMBO reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- Systemic Neutralization of Granulocyte-Macrophage Colony-Stimulating Factor Attenuates Stellate Ganglion Neuroinflammation and Cardiac Sympathetic Overactivation in Chronic Heart Failure in Rats.International journal of molecular sciences · 2026Article
- Hematopoietic and T-lymphopoiesis-stimulating effects of a fluorinated pyrazolopiperidine β-cyclodextrin complex in cyclophosphamide-induced hematopoietic suppression.Frontiers in pharmacology · 2026Article
- Thirty years of NRF2: advances and therapeutic challenges.Nature reviews. Drug discovery · 2025Review
- Endocrine-disrupting compounds and their impact on human placental function: evidence from placenta organ-on-chip studies.Lab on a chip · 2024Article
- [Influence of reactive oxygen species responsive self-assembled nanomicelle loaded with pyroptosis inhibitor on full-thickness skin defects in diabetic rats].Zhonghua shao shang yu chuang mian xiu fu za zhi · 2023Article
- Role of MHC class I pathways inFrontiers in cellular and infection microbiology · 2023Review
- Megakaryocyte NLRP3 hyperactivation induces mild anemia and potentiates inflammatory response in mice.Frontiers in immunology · 2023Article
- GM-CSF suppresses antioxidant signaling and drives IL-1β secretion through NRF2 downregulation.EMBO reports · 2022Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
GM-CSF is a potent inflammatory cytokine regulating myeloid cell differentiation, hematopoiesis, and various other functions. It is functionally associated with a number of inflammatory pathologies including rheumatoid arthritis and inflammatory bowel disease. GM-CSF has been found to promote NLRP3-dependent IL-1β secretion, which may have a significant role in driving inflammatory pathologies. However, the molecular mechanisms remain unknown. Here, we show that GM-CSF induces IL-1β secretion through a ROS-dependent pathway. TNF is required for reactive oxygen species (ROS) generation that strikingly does not promote NLRP3 activation, but instead drives ubiquitylation of IL-1β, promoting its cleavage through basal NRLP3 activity. GM-CSF regulates this pathway through suppression of antioxidant responses via preventing upregulation of NRF2. Thus, the pro-inflammatory effect of GM-CSF on IL-1β is through suppression of antioxidant responses, which leads to ubiquitylation of IL-1β and enhanced processing. This study highlights the role of metabolic regulation of inflammatory signaling and reveals a novel mechanism for GM-CSF to promote inflammation.
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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.