ArticleFrontiers in immunology2023
Lomerizine inhibits LPS-mediated neuroinflammation and tau hyperphosphorylation by modulating NLRP3, DYRK1A, and GSK3α/β.
Article in Frontiers in immunology, 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, 23 citations in OpenAlex.
- Leucettine L41 Ameliorates Tau pathology and neuroinflammation in Parkinson's disease models.BMC neuroscience · 2026Article
- The insulin receptor inhibitor BMS-754807 alleviates neuroinflammation and Alzheimer's disease pathologies across human cellular and mouse models.Journal of neuroinflammation · 2026Article
- Repurposing T-type calcium channel blocker lomerizine as a therapeutic strategy for glioblastoma.JCI insight · 2026Article
- Three-dimensional interactive network: Mitochondrial-metabolic-calcium homeostasis driving Alzheimer's disease.Genes & diseases · 2026Review
- [Aging-Associated Oral Microbiota Dysbiosis and Hypofunction: Their Role in Alzheimer's Disease Pathogenesis].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2026Review
- Glial Cells as Central Players in Neuroinflammation and Neuronal Damage Caused by Bacterial Pneumonia.Neuroimmunomodulation · 2026Review
- A selective agonist of the prostacyclin receptor alleviates microglial and astroglial neuroinflammatory responses through P38 and NLRP3.Frontiers in immunology · 2026Article
- Article
- Calcium signaling hypothesis: A non-negligible pathogenesis in Alzheimer's disease.Journal of advanced research · 2025Review
- Metabolic changes in dorsal root ganglia of newborn Wistar rats following LPS exposure to understand mechanisms of critical illness polyneuropathy.Physiological reports · 2025Article
- Pathological Calcium Signaling in Traumatic Brain Injury and Alzheimer's Disease: From Acute Neuronal Injury to Chronic Neurodegeneration.International journal of molecular sciences · 2025Review
- Sunitinib treatment reduces proinflammatory cytokine levels and mortality rates by suppressing the NLRP3 inflammasome signaling pathway in sepsis.Inflammopharmacology · 2025Article
- Astrocyte priming enhances microglial Aβ clearance and is compromised by APOE4.Nature communications · 2025Article
- Inhibiting NLRP3 Inflammasome Activation to Alleviate Retinal Inflammation and Protect the Optic Nerve of OPTN(E50K)Mice.Inflammation · 2025Article
- Identification of metabolites associated with capecitabine‑induced hand‑foot syndrome using untargeted metabolomics in patients with cancer.Molecular medicine reports · 2025Article
- Enhanced differentiation of neural progenitor cells in Alzheimer's disease into vulnerable immature neurons.iScience · 2025Article
- Imaging lipid rafts reveals the principle of ApoE4-induced Aβ upregulation in human neurons.iScience · 2025Article
- Evaluating metabolic changes in H9c2 cardiomyoblasts exposed to LPS: Towards understanding sepsis mechanisms.PloS one · 2025Article
- Felodipine attenuates neuroinflammatory responses and tau hyperphosphorylation through JNK/P38 signaling in tau-overexpressing AD mice.Molecular brain · 2024Article
- Aspergillusidone G Potentiates the Anti-Inflammatory Effects of Polaprezinc in LPS-Induced BV2 Microglia: A Bioinformatics and Experimental Study.Marine drugs · 2024Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Lomerizine is a calcium channel blocker that crosses the blood-brain barrier and is used clinically in the treatment of migraines. However, whether lomerizine is beneficial in modulating neuroinflammatory responses has not been tested yet. Methods: To assess the potential of lomerizine for repurposing as a treatment for neuroinflammation, we investigated the effects of lomerizine on LPS-induced proinflammatory responses in BV2 microglial cells, Alzheimer's disease (AD) excitatory neurons differentiated from induced pluripotent stem cells (iPSCs), and in LPS-treated wild type mice. Results: In BV2 microglial cells, lomerizine pretreatment significantly reduced LPS-evoked proinflammatory cytokine and NLRP3 mRNA levels. Similarly, lomerizine pretreatment significantly suppressed the increases in Iba-1, GFAP, proinflammatory cytokine and NLRP3 expression induced by LPS in wild-type mice. In addition, lomerizine posttreatment significantly decreased LPS-stimulated proinflammatory cytokine and SOD2 mRNA levels in BV2 microglial cells and/or wild-type mice. In LPS-treated wild-type mice and AD excitatory neurons differentiated from iPSCs, lomerizine pretreatment ameliorated tau hyperphosphorylation. Finally, lomerizine abolished the LPS-mediated activation of GSK3α/β and upregulation of DYRK1A, which is responsible for tau hyperphosphorylation, in wild-type mice. Discussion: These data suggest that lomerizine attenuates LPS-mediated neuroinflammatory responses and tau hyperphosphorylation and is a potential drug for neuroinflammation- or tauopathy-associated diseases.
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