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dc.contributor.authorLucero, Claudia M.
dc.contributor.authorPrieto-Villalobos, Juan
dc.contributor.authorMarambio-Ruiz, Lucas
dc.contributor.authorBalmazabal, Javiera
dc.contributor.authorAlvear, Tanhia F.
dc.contributor.authorVega, Matías
dc.contributor.authorBarra, Paola
dc.contributor.authorRetamal, Mauricio A.
dc.contributor.authorOrellana, Juan A.
dc.contributor.authorGómez, Gonzalo I.
dc.date.accessioned2024-04-10T05:51:38Z
dc.date.available2024-04-10T05:51:38Z
dc.date.issued2022
dc.identifier10.3390/ijms232415936
dc.identifier.issn16616596
dc.identifier.urihttps://hdl.handle.net/20.500.12728/10834
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. © 2022 by the authors.es_ES
dc.description.sponsorshipFondo Nacional de Desarrollo Científico y Tecnológico, FONDECYT, (11200584, 1210375)es_ES
dc.language.isoenes_ES
dc.publisherMDPIes_ES
dc.subjectCa<sup>2+</sup> dynamicses_ES
dc.subjectconnexin 43 hemichanneles_ES
dc.subjectgap junctionses_ES
dc.subjecthypertensive nephropathyes_ES
dc.subjectinflammationes_ES
dc.subjectoxidative stresses_ES
dc.subjectpannexins 1 channelses_ES
dc.titleHypertensive Nephropathy: Unveiling the Possible Involvement of Hemichannels and Pannexonses_ES
dc.typeArticlees_ES


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