ArticleFrontiers in physiology2022
Hypoxia induces purinergic receptor signaling to disrupt endothelial barrier function.
Article in Frontiers in physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- Purinergic signaling in osteoarthritis: Mechanistic insights into pathogenesis and therapeutic targeting.Genes & diseases · 2026Review
- Combined trauma and toxic inhalation in war and disaster medicine: alveolar-capillary barrier failure and respiratory countermeasures.Critical care (London, England) · 2026Review
- Purinergic signaling in dengue infection: modulation of P2 receptors as a potential therapeutic strategy.Purinergic signalling · 2026Review
- P2Y1 receptor in Alzheimer's disease.Neural regeneration research · 2025Article
- Purinergic signaling: A gatekeeper of blood-brain barrier permeation.Frontiers in pharmacology · 2023Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Blood-brain-barrier permeability is regulated by endothelial junctional proteins and is vital in limiting access to and from the blood to the CNS. When stressed, several cells, including endothelial cells, can release nucleotides like ATP and ADP that signal through purinergic receptors on these cells to disrupt BBB permeability. While this process is primarily protective, unrestricted, uncontrolled barrier disruption during injury or inflammation can lead to serious neurological consequences. Purinergic receptors are broadly classified into two families: the P1 adenosine and P2 nucleotide receptors. The P2 receptors are further sub-classified into the P2XR ion channels and the P2YR GPCRs. While ATP mainly activates P2XRs, P2YRs have a broader range of ligand selectivity. The P2Y1R, essential for platelet function, is reportedly ubiquitous in its expression. Prior studies using gene knockout and specific antagonists have shown that these approaches have neuroprotective effects following occlusive stroke. Here we investigated the expression of P2Y1R in primary cultured brain endothelial cells and its relation to the maintenance of BBB function. Results show that following
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Registered trials
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