P2X7 Receptors as a Therapeutic Target in Cerebrovascular Diseases
dc.contributor.author | Cisneros Mejorado, Abraham J. | |
dc.contributor.author | Pérez Samartín, Alberto Luis | |
dc.contributor.author | Domercq García, María | |
dc.contributor.author | Arellano, Rogelio O. | |
dc.contributor.author | Gottlieb, Miroslav | |
dc.contributor.author | Koch Nolte, Friedrich | |
dc.contributor.author | Matute Almau, Carlos José | |
dc.date.accessioned | 2020-11-26T11:00:27Z | |
dc.date.available | 2020-11-26T11:00:27Z | |
dc.date.issued | 2020-06-18 | |
dc.identifier.citation | Frontiers in Molecular Neuroscience 13 : (2020) // Article ID 922 | es_ES |
dc.identifier.issn | 1662-5099 | |
dc.identifier.uri | http://hdl.handle.net/10810/48604 | |
dc.description.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. | es_ES |
dc.description.sponsorship | This study was supported by grants from CONACYT-Mexico No. 252121 and PAPIITUNAM-Mexico No. IN203519 to ROA laboratory; by Spanish Ministry of Education and Science/FEDER (SAF2016-75292-R), Basque Government (IT1203/19), CIBERNED, Eranet-Neuron and Universidad del Pais Vasco to CM's laboratory. AC-M is a researcher from Catedras-CONACYT commissioned at Instituto de Neurobiologia at Universidad Nacional Autonoma de Mexico (UNAM). | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | Frontiers Media | es_ES |
dc.relation | info:eu-repo/grantAgreement/MINECO/SAF2016-75292-R | es_ES |
dc.rights | info:eu-repo/semantics/openAccess | es_ES |
dc.rights.uri | http://creativecommons.org/licenses/by/3.0/es/ | * |
dc.subject | ATP | es_ES |
dc.subject | pannexin-1 | es_ES |
dc.subject | ischemia | es_ES |
dc.subject | neuron | es_ES |
dc.subject | oligodendrocyte | es_ES |
dc.subject | tumor-necrosis-factor | es_ES |
dc.subject | prevents ATP excitotoxicity | es_ES |
dc.subject | oxygen-glucose deprivation | es_ES |
dc.subject | microglial activation | es_ES |
dc.subject | pannexin-1 channels | es_ES |
dc.subject | NLRP3 inflammasomE | es_ES |
dc.subject | IL-1-BETA release | es_ES |
dc.subject | extracellular ATP | es_ES |
dc.subject | TNF-ALPHA | es_ES |
dc.subject | P2X(7) | es_ES |
dc.title | P2X7 Receptors as a Therapeutic Target in Cerebrovascular Diseases | es_ES |
dc.type | info:eu-repo/semantics/article | es_ES |
dc.rights.holder | 2020 Cisneros-Mejorado, Pérez-Samartín, Domercq, Arellano, Gottlieb,Koch-Nolte and Matute. This is an open-access article distributed under the termsof the Creative Commons Attribution License (CC BY). The use, distribution orreproduction in other forums is permitted, provided the original author(s) and thecopyright owner(s) are credited and that the original publication in this journalis cited, in accordance with accepted academic practice. No use, distribution orreproduction is permitted which does not comply with these terms. | es_ES |
dc.rights.holder | Atribución 3.0 España | * |
dc.relation.publisherversion | https://www.frontiersin.org/articles/10.3389/fnmol.2020.00092/full | es_ES |
dc.identifier.doi | 10.3389/fnmol.2020.00092 | |
dc.departamentoes | Neurociencias | es_ES |
dc.departamentoeu | Neurozientziak | es_ES |
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Except where otherwise noted, this item's license is described as 2020 Cisneros-Mejorado, Pérez-Samartín, Domercq, Arellano, Gottlieb,Koch-Nolte and Matute. This is an open-access article distributed under the termsof the Creative Commons Attribution License (CC BY). The use, distribution orreproduction in other forums is permitted, provided the original author(s) and thecopyright owner(s) are credited and that the original publication in this journalis cited, in accordance with accepted academic practice. No use, distribution orreproduction is permitted which does not comply with these terms.