ArticleScientific reports2025
Protein disulfide isomerase integrates toll-like receptor 4 and P2X7 receptor signaling pathways during lipopolysaccharide-induced neuroinflammation.
Article in Scientific reports, 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.
- P2X7 Signaling in Neuroinflammation: Glial Crosstalk, Redox Integration, and Therapeutic Targeting.Journal of molecular neuroscience : MN · 2026Review
- The analgesic effect of electroacupuncture in alleviating paclitaxel-induced peripheral neuropathic pain and its possible mechanism relates to TLR4/P2X7-NLRP3 signaling pathway.Purinergic signalling · 2026Article
- P2X7 Receptor Inhibition Mitigates Microglial Activation, Neuroinflammation, and Secondary Thalamic Damage After Ischemic Stroke.Molecular neurobiology · 2026Article
- Glioblastoma pathophysiology: roles of aging driven changes in STAT3 interactions with NF-κB dimer components in the modulation of the mitochondrial melatonergic pathway and night-time inflammation resolution.Exploration of targeted anti-tumor therapy · 2026Review
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Abstract
P2X7 receptor (P2X7R) augments lipopolysaccharide (LPS)-toll-like receptor 4 (TLR4)-mediated neuroinflammation. These roles of P2X7R in neuroinflammation are relevant to nitrosative stress through nuclear factor-κB (NF-κB)-inducible nitric oxide synthase (iNOS) pathway, while the underlying mechanisms are largely unknown. In the present study, we investigated whether protein disulfide isomerase (PDI) is involved in the integration of TLR4-P2X7R functions in response to LPS in vivo. The present study showed that LPS elicited NF-κB-mediated PDI upregulation, iNOS induction and S-nitrosylated PDI (SNO-PDI) level, independent of S-nitrosylation of NF-κB p65 subunit, in P2X7R
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