Hypertensive Nephropathy: Unveiling the Possible Involvement of Hemichannels and Pannexons

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dc.article.number15936
dc.catalogadorgjm
dc.contributor.authorLucero, Claudia M.
dc.contributor.authorPrieto Villalobos, Juan Carlos
dc.contributor.authorMarambio-Ruiz, Lucas
dc.contributor.authorBalmazabal, Javiera
dc.contributor.authorAlvear Soto, Tanhia Francheska
dc.contributor.authorVega, Matías
dc.contributor.authorBarra, Paola
dc.contributor.authorRetamal, Mauricio A.
dc.contributor.authorOrellana Roca, Juan Andrés
dc.contributor.authorGómez, Gonzalo I.
dc.date.accessioned2024-10-16T15:27:33Z
dc.date.available2024-10-16T15:27:33Z
dc.date.issued2022
dc.description.abstractHypertension is one of the most common risk factors for developing chronic cardiovascular diseases, including hypertensive nephropathy. Within the glomerulus, hypertension causes damage and activation of mesangial cells (MCs), eliciting the production of large amounts of vasoactive and proinflammatory agents. Accordingly, the activation of AT1 receptors by the vasoactive molecule angiotensin II (AngII) contributes to the pathogenesis of renal damage, which is mediated mostly by the dysfunction of intracellular Ca2+ ([Ca2+]i) signaling. Similarly, inflammation entails complex processes, where [Ca2+]i also play crucial roles. Deregulation of this second messenger increases cell damage and promotes fibrosis, reduces renal blood flow, and impairs the glomerular filtration barrier. In vertebrates, [Ca2+]i signaling depends, in part, on the activity of two families of large-pore channels: hemichannels and pannexons. Interestingly, the opening of these channels depends on [Ca2+]i signaling. In this review, we propose that the opening of channels formed by connexins and/or pannexins mediated by AngII induces the ATP release to the extracellular media, with the subsequent activation of purinergic receptors. This process could elicit Ca2+ overload and constitute a feed-forward mechanism, leading to kidney damage.
dc.fechaingreso.objetodigital2024-10-16
dc.format.extent18 páginas
dc.fuente.origenORCID
dc.identifier.doi10.3390/ijms232415936
dc.identifier.issn1422-0067
dc.identifier.pubmedid36555574
dc.identifier.scopusidSCOPUS_ID:85144556571
dc.identifier.urihttps://doi.org/10.3390/ijms232415936
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/88261
dc.identifier.wosidWOS:000902522200001
dc.information.autorucEscuela de Medicina; Prieto Villalobos, Juan Carlos; S/I; 1071673
dc.information.autorucEscuela de Medicina; Alvear Soto, Tanhia Francheska; S/I; 1246198
dc.information.autorucEscuela de Medicina; Orellana Roca, Juan Andrés; 0000-0003-4076-207X; 126007
dc.issue.numero24
dc.language.isoen
dc.nota.accesocontenido completo
dc.relation.ispartofInternational Journal of Molecular Sciences
dc.revistaInternational Journal of Molecular Sciences
dc.rightsacceso abierto
dc.rights.licenseCC BY 4.0 Attribution 4.0 International Deed
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subjectCa2+dynamics
dc.subjectConnexin 43 hemichannel
dc.subjectGap junctions
dc.subjectHypertensive nephropathy
dc.subjectInflammation
dc.subjectOxidative stress
dc.subjectPannexins 1 channels
dc.subject.ddc610
dc.subject.deweyMedicina y saludes_ES
dc.subject.ods03 Good health and well-being
dc.subject.odspa03 Salud y bienestar
dc.titleHypertensive Nephropathy: Unveiling the Possible Involvement of Hemichannels and Pannexons
dc.typeartículo
dc.volumen23
sipa.codpersvinculados1071673
sipa.codpersvinculados1246198
sipa.codpersvinculados126007
sipa.trazabilidadORCID;2024-10-14
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