ArticleFrontiers in neuroscience2020
RAGE Silencing Ameliorates Neuroinflammation by Inhibition of p38-NF-κB Signaling Pathway in Mouse Model of Parkinson's Disease.
Article in Frontiers in neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 49 citations in OpenAlex.
- Trans-spinal magnetic stimulation upregulates microglial SOCS3 to attenuate neuroinflammation in chronic constriction injury-induced neuropathic pain.Neural regeneration research · 2026Article
- Diabetes associated pericyte metabolic signatures and pathogenesis of diabetic retinopathy.Frontiers in endocrinology · 2026Review
- Advanced Glycation End Products Promote PGECells · 2025Article
- Pathway Analysis and Genetic Markers in Parkinson's Disease: Insights into Subtype-Specific Mechanisms.Molecular neurobiology · 2025Article
- Current Evidence on the Involvement of RAGE-Diaph1 Signaling in the Pathology and Treatment of Neurodegenerative Diseases-An Overview.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025Review
- Interaction Between α-Synuclein and DJ-1 in Parkinson's Disease.Brain sciences · 2025Review
- Parkinson's disease: exploring the systemic immune mechanisms through molecular investigations.Inflammopharmacology · 2025Review
- Article
- Potential Applications of Mitochondrial Therapy with a Focus on Parkinson's Disease and Mitochondrial Transplantation.Advanced pharmaceutical bulletin · 2024Review
- Altered expression of Sialyl Lewis X in experimental models of Parkinson's disease.Journal of molecular medicine (Berlin, Germany) · 2024Article
- What Can Inflammation Tell Us about Therapeutic Strategies for Parkinson's Disease?International journal of molecular sciences · 2024Review
- Quantitative Assessment of Intracellular Effectors and Cellular Response in RAGE Activation.Archives of internal medicine research · 2024Article
- Ultra-small polydopamine nanomedicine-enabled antioxidation against senescence.Materials today. Bio · 2023Article
- The link between neuroinflammation and the neurovascular unit in synucleinopathies.Science advances · 2023Review
- Idebenone reduces sepsis-induced oxidative stress and apoptosis in hepatocytes via RAGE/p38 signaling.Annals of translational medicine · 2022Article
- Role of RAGE in the Pathogenesis of Neurological Disorders.Neuroscience bulletin · 2022Review
- Glial Cell-Mediated Neuroinflammation in Alzheimer's Disease.International journal of molecular sciences · 2022Review
- The "Cerebrospinal Fluid Sink Therapeutic Strategy" in Alzheimer's Disease-From Theory to Design of Applied Systems.Biomedicines · 2022Review
- Article
- Pathophysiology of RAGE in inflammatory diseases.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulating evidence suggested that neuroinflammation played a crucial role in dopaminergic neuronal death in Parkinson's disease (PD). The receptor for advanced glycation end products (RAGE), a multi-ligand receptor of the immunoglobulin superfamily, has been proposed as a key molecule in the onset and sustainment of the inflammatory response. Engagement of RAGE contributed to neuroinflammation by upregulating nuclear factor-κB (NF-κB) as well as cytokines. The aim of the present study was to investigate the expression of RAGE in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mice and elucidate the RAGE signal pathway involved in the inflammation. Results showed that RAGE protein and pro-inflammatory cytokines cyclooxygenase type 2 (COX-2) were upregulated in MPTP-treated mice. Further experiments showed that RAGE ablation inhibited phosphorylation of IκB and p38 and protected nigral dopaminergic neurons against cell death in the substantia nigra (SN). These results suggested that RAGE participated in the pathogenesis of PD by neuroinflammation and p38MAPK-NFκB signal pathway may be involved in the process. Moreover, interfering with RAGE signaling pathway may be a reasonable therapeutic option in slowing PD development and progression.
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