Hypertensive Nephropathy: Unveiling the Possible Involvement of Hemichannels and Pannexons

dc.contributor.authorLucero, Claudia
dc.contributor.authorPrieto, Juan
dc.contributor.authorMarambio, Lucas
dc.contributor.authorBalmazabal, Javiera
dc.contributor.authorAlvear, Tanhia
dc.contributor.authorVega, Matías
dc.contributor.authorBarra, Paola
dc.contributor.authorRetamal, Mauricio
dc.contributor.authorOrellana, Juan
dc.contributor.authorGómez, Gonzalo
dc.date.accessioned2023-01-24T15:46:16Z
dc.date.available2023-01-24T15:46:16Z
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.description.versionVersión publicada
dc.identifier.citationLucero CM, Prieto-Villalobos J, Marambio-Ruiz L, Balmazabal J, Alvear TF, Vega M, Barra P, Retamal MA, Orellana JA, Gómez GI. Hypertensive Nephropathy: Unveiling the Possible Involvement of Hemichannels and Pannexons. Int J Mol Sci. 2022 Dec 14;23(24):15936. doi: 10.3390/ijms232415936
dc.identifier.urihttps://doi.org/10.3390/ijms232415936
dc.identifier.urihttps://repositorio.udd.cl/handle/11447/6983
dc.language.isoen
dc.subjectCa2+ dynamics
dc.subjectConnexin 43 hemichannel
dc.subjectGap junctions
dc.subjectHypertensive nephropathy
dc.subjectInflammation
dc.subjectOxidative stress
dc.subjectPannexins 1 channels
dc.titleHypertensive Nephropathy: Unveiling the Possible Involvement of Hemichannels and Pannexons
dc.typeArticle
dcterms.sourceInternational journal of molecular sciences
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