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P2X7 Receptors as a Therapeutic Target in Cerebrovascular Diseases.

Authors
  • Cisneros-Mejorado, Abraham J1
  • Pérez-Samartín, Alberto2
  • Domercq, María2
  • Arellano, Rogelio O1
  • Gottlieb, Miroslav3
  • Koch-Nolte, Friedrich4
  • Matute, Carlos2
  • 1 Instituto de Neurobiología, Universidad Nacional Autónoma de México, Juriquilla, Mexico. , (Mexico)
  • 2 Achucarro Basque Center for Neuroscience, Departamento de Neurociencias, Universidad del País Vasco, CIBERNED, Leioa, Spain. , (Spain)
  • 3 Institute of Neurobiology, Slovak Academy of Sciences, Kosice, Slovakia. , (Slovakia)
  • 4 Department of Immunology, University Hospital, Hamburg, Germany. , (Germany)
Type
Published Article
Journal
Frontiers in Molecular Neuroscience
Publisher
Frontiers Media SA
Publication Date
Jan 01, 2020
Volume
13
Pages
92–92
Identifiers
DOI: 10.3389/fnmol.2020.00092
PMID: 32714144
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Shortage of oxygen and nutrients in the brain induces the release of glutamate and ATP that can cause excitotoxicity and contribute to neuronal and glial damage. Our understanding of the mechanisms of ATP release and toxicity in cerebrovascular diseases is incomplete. This review aims at summarizing current knowledge about the participation of key elements in the ATP-mediated deleterious effects in these pathologies. This includes pannexin-1 hemichannels, calcium homeostasis modulator-1 (CALHM1), purinergic P2X7 receptors, and other intermediaries of CNS injury downstream of ATP release. Available data together with recent pharmacological developments in purinergic signaling may constitute a new opportunity to translate preclinical findings into more effective therapies in cerebrovascular diseases. Copyright © 2020 Cisneros-Mejorado, Pérez-Samartín, Domercq, Arellano, Gottlieb, Koch-Nolte and Matute.

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