ArticleCell host & microbe2025
Methylglyoxal is an antibacterial effector produced by macrophages during infection.
Article in Cell host & microbe, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Antisense transcription reveals disease-associated adaptations in the human gut microbiome.Nature microbiology · 2026Article
- Methylglyoxal AttenuatesInternational journal of molecular sciences · 2026Article
- IFN𝛾 and IFN𝛾 mimetics prevent IFN-I-mediated TB susceptibility by regulating iron metabolism and lipid peroxidation.bioRxiv : the preprint server for biology · 2026Article
- Avoidance of MAIT cells is an essential determinant ofProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Host methylglyoxal activates theProceedings of the National Academy of Sciences of the United States of America · 2026Article
- An Escherichia coli Phosphotransferase System Modulates Methylglyoxal Resistance by Regulating Intracellular Potassium.Molecular microbiology · 2026Article
- Synergistic interactions between glycogen and trehalose mediate adaptation to the stationary phase inJournal of bacteriology · 2026Article
- IL-36γ enhanced bactericidal effects of macrophages to Mycobacterium tuberculosis via the IFN-γ/HIF-1ɑ/glycolysis pathway.Respiratory research · 2026Article
- A putativeFrontiers in immunology · 2026Article
- Cell envelope maintenance by PhoP is essential forProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Bacterial Adaptation to Stress Induced by Glyoxal/Methylglyoxal and Advanced Glycation End Products.Microorganisms · 2025Review
- A glyoxal-specific aldehyde signaling axis in Pseudomonas aeruginosa that influences quorum sensing and infection.Nature communications · 2025Article
- The SGLT2 Inhibitor Empagliflozin Mitigates the Harmful Effects of Methylglyoxal Exposure on Ovalbumin-Induced Mouse Airway Inflammation.International journal of molecular sciences · 2025Article
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10 authors.
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Abstract
Infected macrophages transition into aerobic glycolysis, a metabolic program crucial for controlling bacterial infection. However, antimicrobial mechanisms supported by aerobic glycolysis are unclear. Methylglyoxal is a highly toxic aldehyde that modifies proteins and DNA and is produced as a side product of glycolysis. We show that despite this toxicity, infected macrophages generate high levels of methylglyoxal during aerobic glycolysis while downregulating the detoxification system, including glyoxalase 1 (GLO1). Dampening methylglyoxal generation in mice resulted in enhanced survival of Listeria monocytogenes and Mycobacterium tuberculosis, whereas mice lacking Glo1 have increased methylglyoxal levels and improved infection control. Furthermore, bacteria unable to detoxify methylglyoxal (ΔgloA) exhibit attenuated virulence but are partially rescued in mice that cannot enter glycolysis and generate methylglyoxal. This loss of bacterial GloA results in up to a 1,000-fold greater genomic mutation frequency during infection. Collectively, these results suggest that methylglyoxal is an antimicrobial innate effector that defends against bacterial pathogens.
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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.