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Subject: search.filters.subject.angiotensin ii

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    Angiotensin II-induced pro-fibrotic effects require p38MAPK activity and transforming growth factor beta 1 expression in skeletal muscle cells
    (2012)
    María Gabriela Morales
    ;
    Yaneisi Vazquez
    ;
    María José Acuña
    ;
    Juan Carlos Rivera
    ;
    Felipe Simon
      9Scopus© Citations 77
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    Angiotensin-converting enzyme insertion/deletion polymorphism is associated with severe hypoxemia in pediatric ARDS
    (2011)
    Pablo Cruces
    ;
    Franco Díaz
    ;
    Alonso Puga
    ;
    Benjamín Erranz
    ;
    Alejandro Donoso
    Scopus© Citations 26  1
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    Hypertensive Nephropathy: Unveiling the Possible Involvement of Hemichannels and Pannexons
    (2022)
    Claudia M. Lucero
    ;
    Juan Prieto-Villalobos
    ;
    Lucas Marambio-Ruiz
    ;
    Javiera Balmazabal
    ;
    Tanhia F. Alvear
    <jats:p>Hypertension 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.</jats:p>
      5Scopus© Citations 18