ArticleMolecular neurodegeneration2025
Inactivation of NLRP3 inflammasome by dephosphorylation at Serine 658 alleviates glial inflammation in the mouse model of Parkinson's disease.
Article in Molecular neurodegeneration, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Natural Neurobiological Active Compounds in Parkinson's Disease: Molecular Targets, Signaling Pathways, and Therapeutic Prospects.International journal of molecular sciences · 2026Pooled it
- The impact of post-translational modifications and subcellular localization on NLRP3 inflammasome activation: A systematic review.Cell communication and signaling : CCS · 2025Pooled it
- Bioactivity-guided optimization of Gastrodia elata cultivation: integrated modulation of spawn wood length, tree species and pit size.Journal of natural medicines · 2026Article
- Cascade-targeted intervention of the NLRP3 inflammasome and downstream angiogenesis by curcumin nanoparticles for ocular neovascularization therapy.Clinical and translational medicine · 2026Article
- The NLRP3 inflammasome: pathophysiology and therapeutic implications for schizophrenia and neuropsychiatric disorders.Molecular psychiatry · 2026Review
- Inhibition of HSPA8 alleviates experimental autoimmune encephalomyelitis via dual modulation of NLRP3 inflammasome activation: suppressing both NF-κB-mediated priming and ASC-dependent assembly.Cell death discovery · 2026Article
- The vicious cycle: unraveling the interplay between α-synuclein, mitochondrial dysfunction, and neuroinflammation in Parkinson's disease.Journal of neurology · 2026Review
- Ginsenoside Rg2 attenuates secondary brain injury following intracerebral hemorrhage by inhibiting NLRP3-mediated pyroptosis.Journal of neuroinflammation · 2026Article
- Alternative Pathway for Methyl Supply through the Coupling of SHMT1 and PEMT to Maintain Astrocytic Homeostasis in Parkinson's Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Exploring the nexus between inflammation and mobility through the lens of healthy aging: current scenario and future perspectives.Aging clinical and experimental research · 2026Review
- Microglia, Astrocytes, and Oligodendrocytes in Parkinson's Disease: Neuroinflammatory Crosstalk and Emerging Therapeutic Strategies.Biomolecules · 2026Review
- Mitophagy-NLRP3 Inflammasome Crosstalk in Parkinson's Disease: Pathogenic Mechanisms and Emerging Therapeutic Strategies.International journal of molecular sciences · 2026Review
- The NLRP3-α-Synuclein Circuit: A Core Driver and Therapeutic Target in Parkinson's Disease.Journal of inflammation research · 2026Review
- Chronic Styrene Exposure Causes Oxidative Stress, Neuroinflammation, and Hippocampal Memory Dysfunction via NLRP3 Inflammasome Activation.Molecular neurobiology · 2025Article
- Neuronal FGF13 Inhibits Mitochondria-Derived Damage Signals to Prevent Neuroinflammation and Neurodegeneration in a Mouse Model of Parkinson's Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Exercise regulates mitophagy to alleviate parkinsonian neurodegeneration.Frontiers in aging neuroscience · 2025Review
- Spatiotemporal crosstalk among mitochondrial dynamics, NLRP3 inflammasome activation, and histone lactylation drivesFrontiers in cellular neuroscience · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
backgroundParkinson's disease (PD) is a leading neurodegenerative disorder characterized by the progressive loss of dopaminergic neurons, contributing to considerable disability worldwide. Current treatments offer only symptomatic relief, highlighting the need for novel therapeutic strategies targeting disease progression. Neuroinflammation plays a pivotal role in PD pathogenesis, with the NLRP3 inflammasome emerging as a key contributor.
methodsThe virtual screening of a natural product library comprising 5,088 compounds was applied to identify five potential NLRP3 inhibitors through molecular docking scores. Then surface plasmon resonance assays were used to detect their binding affinities to the NLRP3 protein. Functional studies in macrophages and glial cells were used to demonstrate the effect of Psoralen on NLRP3 phosphorylation and inflammasome activation.
resultsPsoralen treatment improved PD-like symptoms and reduced dopaminergic neuronal death by targeting glial NLRP3 inflammasome activation in the MPTP/p mouse model. By performing 4D label-free quantitative phosphorylation proteomics and site mutation assays, we identified that Psoralen prevents NLRP3 phosphorylation at Serine 658 by binding to its NACHT and LRR domains.
conclusionsThese findings position Psoralen as a promising NLRP3 inflammasome inhibitor, offering a potential therapeutic avenue for PD and other NLRP3 inflammasome-related diseases. Additionally, this research highlights the innovative approach of targeting specific phosphorylation sites on the NLRP3 protein to reduce neuroinflammation.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.