Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/9691
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dc.contributor.authorGalani, V.en
dc.contributor.authorTatsaki, E.en
dc.contributor.authorBai, M.en
dc.contributor.authorKitsoulis, P.en
dc.contributor.authorLekka, M.en
dc.contributor.authorNakos, G.en
dc.contributor.authorKanavaros, P.en
dc.date.accessioned2015-11-24T16:51:07Z-
dc.date.available2015-11-24T16:51:07Z-
dc.identifier.issn0344-0338-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/9691-
dc.rightsDefault Licence-
dc.subjectacute respiratory distress syndromeen
dc.subjectapoptosisen
dc.subjectepithelial cellsen
dc.subjectneutrophilsen
dc.subjectacute lung injuryen
dc.subjectcolony-stimulating factoren
dc.subjectnf-kappa-ben
dc.subjectartery endothelial-cellsen
dc.subjectfas/fas ligand systemen
dc.subjecthuman fas liganden
dc.subjectneutrophil apoptosisen
dc.subjectepithelial-cellsen
dc.subjectmediated cytotoxicityen
dc.subjectextracellular atpen
dc.titleThe role of apoptosis in the pathophysiology of Acute Respiratory Distress Syndrome (ARDS): An up-to-date cell-specific reviewen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.primaryDOI 10.1016/j.prp.2009.12.002-
heal.identifier.secondary<Go to ISI>://000276208100001-
heal.identifier.secondaryhttp://ac.els-cdn.com/S0344033809002982/1-s2.0-S0344033809002982-main.pdf?_tid=4d00a1a471f02014928c4ddf4642287a&acdnat=1333033637_a79c14aeaf8d8ca49e0b58324d45079b-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Θετικών Επιστημών. Τμήμα Χημείαςel
heal.publicationDate2010-
heal.abstractARDS pathophysiology is characterized by complex mechanisms that involve cells of inflammation, lung tissue cells, cytokines, chemokines, as well as apoptosis activators and inhibitors. There are two important theories that link apoptosis with ARDS and suggest that epithelial cell apoptosis, as well as the accumulation of neutrophils in the lung, may contribute to a cascade of events and, finally, ARDS. The activation of the Fas/FasL pathway is an important mechanism of alveolar epithelial injury in the lungs of patients with ALI. In addition, neutrophilic inflammation in the alveolar spaces is characteristic of ALI in humans and in most animal models of ALI. The enhanced phagocytosis of apoptotic neutrophils could lead to resolution of inflammation and repair during ARDS. In this review, we will focus on elucidating the role of apoptosis in the pathophysiology of ARDS and the contribution of Fas-mediated inflammation in ARDS. Furthermore, we will give evidence that TNF-alpha, IL-1beta and IL-13 attenuate the pro-cell death effects of Fas/CD95 on A549 epithelial cells, at least partially, by the NF-kB and PI3-K pathways, suggesting that induction of the expression of antiapoptotic genes protects the epithelial cells from cell death. (c) 2009 Elsevier GmbH. All rights reserved.en
heal.publisherElsevieren
heal.journalNamePathology Research and Practiceen
heal.journalTypepeer reviewed-
heal.fullTextAvailabilityTRUE-
Appears in Collections:Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά). ΧΗΜ

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