ArticleAging2022
Inhibition of NLRP3 and Golph3 ameliorates diabetes-induced neuroinflammation
Article in Aging, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 13 citations in OpenAlex.
- Hyperglycemia-induced overexpression of CREB3 L3 promotes the epithelial-to-mesenchymal transition in bladder urothelial cells in diabetes mellitus.World journal of diabetes · 2025Article
- GOLPH3 promotes calcium oxalate-induced renal injury and fibrosis through Golgi stress-mediated apoptosis and inflammatory responses.Scientific reports · 2025Article
- Machine learning analysis of gene expression profiles of pyroptosis-related differentially expressed genes in ischemic stroke revealed potential targets for drug repurposing.Scientific reports · 2025Article
- Comprehensive Analysis of circRNA and mRNA Revealing Potential Mechanism Underlying Neuroinflammation in BV2 Cells.Endocrine, metabolic & immune disorders drug targets · 2025Article
- Emerging Evidence of Golgi Stress Signaling for Neuropathies.Neurology international · 2024Review
- GOLPH3 promotes endotoxemia-induced liver and kidney injury through Golgi stress-mediated apoptosis and inflammatory response.Cell death & disease · 2023Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Golgi stress has been observed in various neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease. Whether Golgi stress participates in hyperglycemia-induced neuroinflammation, and how it is regulated remain unclear. First, we found that high glucose (HG) could induce dispersed Golgi apparatus (GA) in BV2 cells, which can be reversed by knockout of NLRP3. Next, we discovered that HG could promote the interaction of NLRP3 and VPS35 and then enhances the interaction of VPS35 and Golph3; knockout of NLRP3 suppressed the expression of VPS35 and Golph3; knockout of VPS35 reduced the expression of Golph3 but not NLRP3, indicating that HG induced the activation of NLRP3/VPS35/Golph3 pathway in BV2 cells. Further, we elucidated the signaling pathway that Golph3 mediated GA stress in HG condition. We used GST-pulldown and Co-IP experiments methods to show that HG promoted the interaction of Golph3 and Vimentin, knockout of Golph3 alleviated the expression of Vimentin. Knockout out of Golph3 and Vimentin both ameliorated HG induced dispersed Golgi apparatus. Collectively, our study demonstrated that HG regulates GA stress through NLRP3/VPS35/Golph3/Vimentin pathway. At last, we found that a combination of small molecular inhibitors targeting NLRP3 and Golph3 selected by molecular docking could alleviate HG-induced neuroinflammation
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