ArticleJournal of neuroinflammation2023
NOD-like receptor NLRC5 promotes neuroinflammation and inhibits neuronal survival in Parkinson's disease models.
Article in Journal of neuroinflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 37 citations in OpenAlex.
- NLRC5 restricts Japanese encephalitis virus replication and neuroinflammation by interacting with the viral NS3 protein in an IFN-γ-dependent manner.Journal of neuroinflammation · 2026Article
- Sex-dependent impact ofGenes & diseases · 2026Article
- Neuroinflammation promotes the development of pharmacoresistant epilepsy by triggering the MSK1/CREB signaling pathway.Scientific reports · 2026Article
- Laminarin attenuates neuroinflammation in MPTP-induced Parkinson's disease mouse model via inhibiting dectin-1/Syk/NF-κB signaling.Inflammopharmacology · 2026Article
- Microglia, Astrocytes, and Oligodendrocytes in Parkinson's Disease: Neuroinflammatory Crosstalk and Emerging Therapeutic Strategies.Biomolecules · 2026Review
- Microglia heterogeneity and therapeutic strategies in Parkinson's disease.Frontiers in immunology · 2026Review
- Diet-Driven Microglial Activation: Region-Specific Neuroinflammation in the Mouse Brain.Brain sciences · 2025Article
- NLRC5-Mediated Epigenetic and Proteomic Regulation of Microglial Panoptosis Drives Neuroinflammation in Multiple Sclerosis.Molecular neurobiology · 2025Article
- Microglial NLRC5 drives lysosomal dysfunction to disrupt autophagic flux and promote post-stroke neuroinflammation.Journal of neuroinflammation · 2025Article
- O-GlcNAcylation Mediated by OGA Activates NEK7/NLRP3 Pathway to Promote Pyroptosis in Parkinson's Disease.Journal of cellular and molecular medicine · 2025Article
- New insights into the structure domain and function of NLR family CARD domain containing 5.Cell communication and signaling : CCS · 2025Review
- Interleukin-6 in epilepsy and its neuropsychiatric comorbidities: How to bridge the gap.World journal of psychiatry · 2025Article
- Astrocyte-mediated inflammatory responses in traumatic brain injury: mechanisms and potential interventions.Frontiers in immunology · 2025Review
- Extracellular Vesicles Derived from FGF2-Primed Astrocytes Against Mitochondrial and Synaptic Toxicities in Parkinson's Disease.International journal of nanomedicine · 2025Article
- Hyperbaric Oxygen Therapy Reduces the Traumatic Brain Injury-Mediated Neuroinflammation Through Enrichment of Prevotella Copri in the Gut of Male Rats.Neurocritical care · 2024Article
- GSK3-Driven Modulation of Inflammation and Tissue Integrity in the Animal Model.International journal of molecular sciences · 2024Review
- The potential role of brain renin-angiotensin system in the neuropathology of Parkinson disease: Friend, foe or turncoat?Journal of cellular and molecular medicine · 2024Review
- BDNF/TrkB activators in Parkinson's disease: A new therapeutic strategy.Journal of cellular and molecular medicine · 2024Review
- Hypoxia inducible factor-1α regulates microglial innate immune memory and the pathology of Parkinson's disease.Journal of neuroinflammation · 2024Article
- NLRC5 Deficiency Reduces LPS-Induced Microglial Activation via Inhibition of NF-κB Signaling and Ameliorates Mice's Depressive-like Behavior.International journal of molecular sciences · 2023Article
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Authors and funding
17 authors at 5 institutions in 1 country.
Funding
Abstract
Parkinson's disease (PD) is mainly characterized by the progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNpc) and neuroinflammation mediated by overactivated microglia and astrocytes. NLRC5 (nucleotide-binding oligomerization domain-like receptor family caspase recruitment domain containing 5) has been reported to participate in various immune disorders, but its role in neurodegenerative diseases remains unclear. In the current study, we found that the expression of NLRC5 was increased in the nigrostriatal axis of mice with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine hydrochloride (MPTP)-induced PD, as well as in primary astrocytes, microglia and neurons exposed to different neurotoxic stimuli. In an acute MPTP-induced PD model, NLRC5 deficiency significantly reduced dopaminergic system degeneration and ameliorated motor deficits and striatal inflammation. Furthermore, we found that NLRC5 deficiency decreased the expression of the proinflammatory genes IL-1β, IL-6, TNF-α and COX2 in primary microglia and primary astrocytes treated with neuroinflammatory stimuli and reduced the inflammatory response in mixed glial cells in response to LPS treatment. Moreover, NLRC5 deficiency suppressed activation of the NF-κB and MAPK signaling pathways and enhanced the activation of AKT-GSK-3β and AMPK signaling in mixed glial cells. Furthermore, NLRC5 deficiency increased the survival of primary neurons treated with MPP
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