ArticleCell reports2024
The glycolytic metabolite methylglyoxal covalently inactivates the NLRP3 inflammasome.
Article in Cell reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Methylglyoxal-modification of NLRP3 interrupts NLRP3-NEK7 interaction diminishing inflammasome activation and neuroinflammation.Journal of neuroinflammation · 2026Article
- Role of Glycolysis and Nitric Oxide Pathway Crosstalk in Macrophages in Atherosclerosis.Current medicinal chemistry · 2026Review
- Uncovering the mechanisms of homologous point acupuncture on knee osteoarthritis through an integrated study of metabolomics and proteomics.Frontiers in bioengineering and biotechnology · 2026Article
- Isotope Dilution nanoLC-MS/MS Quantitation of Methylglyoxal DNA-Protein Crosslinks: Formation and Repair in Human Cells.bioRxiv : the preprint server for biology · 2025Article
- The Glycolysis-HIF-1α axis induces IL-1β of macrophages in rheumatoid arthritis.Arthritis research & therapy · 2025Article
- Optimizing PDIA1 Inhibition as a Strategy to Inhibit NLRP3 Inflammasome Activation and Activity.ACS chemical biology · 2025Article
- Inhibition of NF-κB Signaling by the Reactive Glycolytic Metabolite Methylglyoxal.bioRxiv : the preprint server for biology · 2025Article
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8 authors.
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Abstract
The NLRP3 inflammasome promotes inflammation in disease, yet the full repertoire of mechanisms regulating its activity is not well delineated. Among established regulatory mechanisms, covalent modification of NLRP3 has emerged as a common route for the pharmacological inactivation of this protein. Here, we show that inhibition of the glycolytic enzyme phosphoglycerate kinase 1 (PGK1) results in the accumulation of methylglyoxal, a reactive metabolite whose increased levels decrease NLRP3 assembly and inflammatory signaling in cells. We find that methylglyoxal inactivates NLRP3 via a non-enzymatic, covalent-crosslinking-based mechanism, promoting inter- and intraprotein MICA (methyl imidazole crosslink between cysteine and arginine) posttranslational linkages within NLRP3. This work establishes NLRP3 as capable of sensing a host of electrophilic chemicals, both exogenous small molecules and endogenous reactive metabolites, and suggests a mechanism by which glycolytic flux can moderate the activation status of a central inflammatory signaling pathway.
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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 Socratic graph.