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dc.contributor.authorGarcía-Rodríguez, Carmenes_ES
dc.contributor.authorParra Izquierdo, Ivánes_ES
dc.contributor.authorCastaños-Mollor, Irenees_ES
dc.contributor.authorLópez, Javieres_ES
dc.contributor.authorSan Román, José Albertoes_ES
dc.contributor.authorSánchez Crespo, Marianoes_ES
dc.date.accessioned2019-12-18T08:16:45Z-
dc.date.available2019-12-18T08:16:45Z-
dc.date.issued2018-
dc.identifier.citationFrontiers in Physiology 9: 201 (2018)es_ES
dc.identifier.urihttp://hdl.handle.net/10261/196958-
dc.description.abstractInflammation, the primary response of innate immunity, is essential to initiate the calcification process underlying calcific aortic valve disease (CAVD), the most prevalent valvulopathy in Western countries. The pathogenesis of CAVD is multifactorial and includes inflammation, hemodynamic factors, fibrosis, and active calcification. In the development of CAVD, both innate and adaptive immune responses are activated, and accumulating evidences show the central role of inflammation in the initiation and propagation phases of the disease, being the function of Toll-like receptors (TLR) particularly relevant. These receptors act as sentinels of the innate immune system by recognizing pattern molecules from both pathogens and host-derived molecules released after tissue damage. TLR mediate inflammation via NF-κB routes within and beyond the immune system, and play a crucial role in the control of infection and the maintenance of tissue homeostasis. This review outlines the current notions about the association between TLR signaling and the ensuing development of inflammation and fibrocalcific remodeling in the pathogenesis of CAVD. Recent data provide new insights into the inflammatory and osteogenic responses underlying the disease and further support the hypothesis that inflammation plays a mechanistic role in the initiation and progression of CAVD. These findings make TLR signaling a potential target for therapeutic intervention in CAVD.es_ES
dc.description.sponsorshipSources of funding include grants from the Instituto de Salud Carlos III (Spanish Ministry of Health): PI14/00022, CIBERCV; the Ministry of Economy and Competitivity of Spain, cofunded by the European Social Fund: SAF2013-44521-R; Junta de Castilla y León: GRS 1432/A/16, BIO/VA47/14, BIO/VA36/15, CSI035P17; Fundación Domingo Martínez. IP-I was a fellow from the University of Valladolid co-funded by Banco de Santander; IC-M was supported by a pre-doctoral fellowship from Regional Government of Castilla y León and the European Social Fund co-funded by CSIC.es_ES
dc.language.isoenges_ES
dc.publisherFrontiers Mediaes_ES
dc.relationMINECO/ICTI2013-2016/SAF2013-44521-Res_ES
dc.relation.isversionofPublisher's versiones_ES
dc.rightsopenAccesses_ES
dc.subjectNF-κBes_ES
dc.subjectToll-like receptor (TLR)es_ES
dc.subjectAortic valve interstitial cell (VIC)es_ES
dc.subjectCalcific aortic valve disease (CAVD)es_ES
dc.titleToll-like receptors, inflammation, and calcific aortic valve diseasees_ES
dc.typeartículoes_ES
dc.identifier.doi10.3389/fphys.2018.00201-
dc.description.peerreviewedPeer reviewedes_ES
dc.relation.publisherversionhttps://doi.org/10.3389/fphys.2018.00201es_ES
dc.identifier.e-issn1664-042X-
dc.rights.licensehttp://creativecommons.org/licenses/by/4.0/es_ES
dc.contributor.funderInstituto de Salud Carlos IIIes_ES
dc.contributor.funderMinisterio de Economía y Competitividad (España)es_ES
dc.contributor.funderEuropean Commissiones_ES
dc.contributor.funderUniversidad de Valladolides_ES
dc.contributor.funderFundación Domingo Martínezes_ES
dc.contributor.funderBanco Santanderes_ES
dc.contributor.funderJunta de Castilla y Leónes_ES
dc.contributor.funderConsejo Superior de Investigaciones Científicas (España)es_ES
dc.relation.csices_ES
oprm.item.hasRevisionno ko 0 false*
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dc.identifier.funderhttp://dx.doi.org/10.13039/100010784es_ES
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dc.identifier.funderhttp://dx.doi.org/10.13039/501100003339es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100000780es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100003329es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100007515es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/100010784es_ES
dc.identifier.pmid29593562-
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