P2X7 Receptors as a Therapeutic Target in Cerebrovascular Diseases

Abraham J Cisneros-Mejorado; Alberto Pérez-Samartín; María Domercq; Rogelio O Arellano; Miroslav Gottlieb; Friedrich Koch-Nolte; Carlos Matute

doi:10.3389/fnmol.2020.00092

P2X7 Receptors as a Therapeutic Target in Cerebrovascular Diseases

Front Mol Neurosci. 2020 Jun 18:13:92. doi: 10.3389/fnmol.2020.00092. eCollection 2020.

Authors

Abraham J Cisneros-Mejorado¹, Alberto Pérez-Samartín², María Domercq², Rogelio O Arellano¹, Miroslav Gottlieb³, Friedrich Koch-Nolte⁴, Carlos Matute²

Affiliations

¹ Instituto de Neurobiología, Universidad Nacional Autónoma de México, Juriquilla, Mexico.
² Achucarro Basque Center for Neuroscience, Departamento de Neurociencias, Universidad del País Vasco, CIBERNED, Leioa, Spain.
³ Institute of Neurobiology, Slovak Academy of Sciences, Kosice, Slovakia.
⁴ Department of Immunology, University Hospital, Hamburg, Germany.

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.

Keywords: ATP; ischemia; neuron; oligodendrocyte; pannexin-1.