ArticleFrontiers in immunology2025
ATP/P2X7 receptor signal aggravates ischemic stroke injury by activating Th17 cells via STAT3/IL-21 pathway.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- From metabolic intermediary to neurotransmitter: purinergic signaling in neurophysiology and vulnerability of brain circuits.Bioscience reports · 2026Review
- P2X7 Signaling in Neuroinflammation: Glial Crosstalk, Redox Integration, and Therapeutic Targeting.Journal of molecular neuroscience : MN · 2026Review
- Nucleotide Metabolism in Health and Disease.MedComm · 2026Review
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Authors and funding
9 authors.
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Abstract
Background: During cerebral ischemia, adenosine triphosphate (ATP) is released into the extracellular matrix from damaged neurons and glial cells, functioning as a danger signal. However, the involvement of ATP/P2X7 signaling in regulating the infiltrated lymphocytes during ischemia-reperfusion (IR) injury remain unclear. Methods: The expression level of P2X7 was evaluated in infiltrated lymphocytes from experimental stroke mice. To further elucidate the role of P2X7 signaling in infiltrated immune cells during ischemic stroke, P2X7-knockout (KO) mice and Rag2 Results: Flow cytometry analysis revealed that the expression of P2X7 was mainly expressed in CD4 Conclusions: Our findings suggest that the loss of ATP/P2X7 signaling in CD4
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