ArticleImmunity, inflammation and disease2025
IGF2BP2 Regulates the Progression of Alzheimer's Disease Through m6A-Mediated NLRP3 Inflammasome.
Article in Immunity, inflammation and disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Brain-targeted delivery of siRNA via non-viral delivery systems, the therapeutic strategy for Alzheimer's disease-Unveiling challenges and prospects.International journal of pharmaceutics: X · 2026Review
- Melatonin Alleviates Cerebral Ischemia/Reperfusion Injury by Mitigating AIM2-Mediated PANoptosis in Ischemic Penumbra.Molecular neurobiology · 2026Article
- Histone Lactylation Contributes to Neuropathic Pain by Facilitating mThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Pyroptosis Regulated by N6-Methyladenosine Modification: Implications for Pyroptosis-Related Disease Therapy.Journal of innate immunity · 2026Review
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Authors and funding
4 authors.
Funding
Abstract
backgroundRecent studies show that N6-methyladenosine (m6A) plays an important role in the pathogenesis of the Alzheimer's disease (AD), while the mechanisms involved were studied insufficiently.
aimsThe present study aimed to explore the effect of human insulin-like growth factor 2 (IGF2) mRNA binding proteins 2 (IGF2BP2), one of the m6A-binding proteins on the progression of AD. MATERIALS &
methodsThe mRNA and protein expression level were determined using RT-qPCR and western blot, respectively. MTT assay was carried out to evaluate cell viability. The content of ROS, antioxidant enzymes, IL-1β and pyroptosis, as well as m6A contents were determined using relative commercial kit. The AD models were built using Aβ1-42 -stimulated hippocampal neuron in vitro and AD mice in vivo.
resultsOur results showed that IGF2BP2 was significantly upregulated in the Aβ1-42 -stimulated hippocampal neuron. IGF2BP2 inhibition reversed the decreased cell viability and the increased cell apoptosis induced by Aβ1-42. IGF2BP2 siRNA transfection alleviated Aβ1-42 induced pyroptosis and pyroptosis-related proteins upregulation. we also found that IGF2BP2 inhibition downregulated the expression of NLRP3 through m6A methylation. Furthermore, overexpression of NLRP3 partly reversed the effect of IGF2BP2 inhibition on Aβ1-42 -induced hippocampal neuron injury. In addition, IGF2BP2 improved cognitive function and alleviated Aβ1-42 neuronal injury in vivo.
conclusionKnockdown of IGF2BP2 inhibit neuronal damage and pyroptosis in the hippocampus cells, and improve cognitive function in AD partly through m6A-mediated NLRP3 inflammasome.
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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 Socratic graph.