ArticleCellular & molecular immunology2024
GSNOR negatively regulates the NLRP3 inflammasome via S-nitrosation of MAPK14.
Article in Cellular & molecular immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.
- The impact of post-translational modifications and subcellular localization on NLRP3 inflammasome activation: A systematic review.Cell communication and signaling : CCS · 2025Pooled it
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- Spatiotemporal iron-hijacking hydrogel reprograms host-pathogen iron homeostasis for fungal keratitis therapy.Cell reports. Medicine · 2026Article
- Exploring the Therapeutic Effects ofPharmaceuticals (Basel, Switzerland) · 2026Article
- Pharmaceutical therapies for pyroptosis in lung injury.Inflammopharmacology · 2026Review
- Potential mechanisms of natural products in improving gouty arthritis: Focusing on NLRP3 inflammasome regulation.Journal of pharmaceutical analysis · 2026Review
- TIGAR regulates intestinal mucus barrier integrity by inhibiting lactylation of G6PD/6PGD in ulcerative colitis.Nature communications · 2026Article
- Interpretable machine learning identifies a clinically inferred inflammasome-associated inflammatory injury phenotype in children with adenovirus pneumonia.Frontiers in cellular and infection microbiology · 2026Article
- In vivo chemogenetic RNA editing of macrophages by bioengineered viruses for sepsis treatment.Nature communications · 2025Article
- Article
- Updated insights into the molecular networks for NLRP3 inflammasome activation.Cellular & molecular immunology · 2025Review
- Early transcriptional and cellular abnormalities in choroid plexus of a mouse model of Alzheimer's disease.Molecular neurodegeneration · 2025Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hyperactivation of the NLRP3 inflammasome has been implicated in the pathogenesis of numerous diseases. However, the precise molecular mechanisms that modulate the transcriptional regulation of NLRP3 remain largely unknown. In this study, we demonstrated that S-nitrosoglutathione reductase (GSNOR) deficiency in macrophages leads to significant increases in the Nlrp3 and Il-1β expression levels and interleukin-1β (IL-1β) secretion in response to NLRP3 inflammasome stimulation. Furthermore, in vivo experiments utilizing Gsnor
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