Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/23331
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dc.contributor.authorTsatsoulis, A.en
dc.date.accessioned2015-11-24T19:31:50Z-
dc.date.available2015-11-24T19:31:50Z-
dc.identifier.issn0026-4806-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/23331-
dc.rightsDefault Licence-
dc.subjectAntigens, CD95/metabolismen
dc.subjectApoptosis/*physiologyen
dc.subjectApoptosis Regulatory Proteinsen
dc.subjectFas Ligand Proteinen
dc.subjectGoiter/*pathology/physiopathologyen
dc.subjectHumansen
dc.subjectMembrane Glycoproteins/metabolismen
dc.subjectTNF-Related Apoptosis-Inducing Liganden
dc.subjectThyroid Neoplasms/pathology/physiopathologyen
dc.subjectThyroiditis, Autoimmune/*pathology/physiopathologyen
dc.subjectTumor Necrosis Factor-alpha/metabolismen
dc.titleThe role of apoptosis in thyroid diseaseen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/12094148-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate2002-
heal.abstractIncreasing evidence suggests that apoptosis plays an important role in the pathogenesis of autoimmune and proliferative thyroid diseases, and that the apoptotic pathways involved are complex and highly regulated. Autoimmune thyroid diseases such as Hashimoto's thyroiditis and Graves' disease have been associated with differential expression of Fas and TRAIL receptor-mediated apoptosis. Thus, the thyroid cell destruction characteristic of autoimmune thyroiditis can be seen as the consequence of inappropriate expression of Fas or TRAIL death pathway molecules and down-regulation of the apoptosis controlling protein Bcl-2, which may be induced by cytokines released locally by infiltrating lymphocytes. In contrast, Graves' thyrocytes are protected from apoptotic death possibly by the anti-apoptotic action of thyrotrophin receptor antibodies or soluble Fas and/or the overexpression of Fas ligand which all create an anti-apoptotic potential for the thyroid cells and favor apoptosis of the infiltrating lymphocytes. On the other hand, an imbalance between thyroid cell proliferation and cell death may be crucial for goiter formation or cancer development and progression. In human thyroid goiter, Fas-mediated apoptosis is suppressed, leading to thyroid cell hyperplasia. Furthermore, malignant thyroid cells may escape immune attack by over expressing Fas ligand and inducing apoptosis in the invading immune cells. However, the exact mechanisms involved in the regulation of apoptosis in thyroid disease remain unclear. Further investigation is needed that may provide new strategies in the prevention and treatment of these diseases.en
heal.journalNameMinerva Meden
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
Appears in Collections:Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) - ΙΑΤ

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