ArticleFrontiers in immunology2025
MicroRNA-132 regulates quinolinic acid production in the brain during LPS-induced neuroinflammation.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- The Kynurenine Pathway: Unraveling Its Role in Neurological Disorders via Mammalian Cellular Models.International journal of molecular sciences · 2026Review
- The kynurenine pathway storm in epilepsy: mechanisms and therapeutic implications.Acta epileptologica · 2026Review
- Kynurenine Pathway, Nrf2 and NF-κB Cross-Regulation in the CNS: An Overview.Molecular neurobiology · 2026Review
- The role of the kynurenine pathway in conditioned place aversion induced by synthetic cannabinoid CP-55940.Behavioral and brain functions : BBF · 2026Article
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Authors and funding
6 authors.
Funding
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Abstract
Background: The kynurenine pathway (KP) plays a major role in neuroinflammation by converting the amino acid tryptophan into a variety of neuroactive products, including neurotoxic quinolinic acid (QUIN). The gene expression regulatory role of microRNAs in neuroinflammation is well documented; however, their impact on KP in the brain remains unexplored. Methods: In this study, we investigated whether the neuroimmune miR-132/212 cluster regulates one or more members of the KP during lipopolysaccharide (LPS)-induced neuroinflammation Results: In wildtype mice, we demonstrated that a subtoxic dose of LPS triggers a significant neuroinflammatory response with upregulation of KP enzymes, particularly kynurenine 3-monooxygenase (KMO), a key enzyme in QUIN synthesis, leading to elevated brain levels of this neurotoxic metabolite. Interestingly, KMO expression and activity remained elevated in miR-132/212 knockout mice after post-inflammation resolution. Conclusion: Collectively, these findings suggest that the miR-132/212 cluster functions as a novel modulator of KP metabolism during LPS-induced inflammation, and acts as a potential therapeutic target for controlling neurotoxic QUIN accumulation in neuroinflammatory conditions.
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