Title | Apoptosis and the pathogenesis of Hashimoto’s thyroiditis | |
Authors | George Mastorakos¹, Ioannis Ilias¹ and Nicholas Mitsiades²
1. Endocrine Unit, Evgenidion Hospital, University of Athens, Greece 2. Developmental Endocrinology Branch, National Institutes of Health, Bethesda, Maryland, USA |
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Citation | Mastorakos, G., Ilias, I., Mitsiades, N.: Apoptosis and the pathogenesis of Hashimoto’s thyroiditis, Epitheorese Klin. Farmakol. Farmakokinet. 14(1): 19-24 (2000) | |
Publication Date | Received for publication: 6 December 1999
Accepted for publication: 10 December 1999 |
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Full Text Language | English | |
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Keywords | Hashimoto’s thyroiditis, pathogenesis, apoptosis. | |
Other Terms | review article | |
Summary | The Fas protein, its ligand FasL and the Bcl-2 gene play major roles in apoptosis. Follicular cells in Hashimoto’s thyroiditis undergo apoptosis by concomitant upregulation of FasL and Fas and downregulation of Bcl-2 proteins. Autoimmune disorders with epithelial cell destruction, including Hashimoto’s thyroiditis, might share a common pathophysiology by which the target cells are engaged in a suicidal / fratricidal mode of death involving Fas /FasL interaction. Therapeutic interventions on genes involved in central cell death can be envisaged. | |
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Online ISSN 1011-6575
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Articles published in this Journal are Indexed or Abstracted in: • Chemical Abstracts • Elsevier’s Bibliographic Databases: Scopus, EMBASE, EMBiology, Elsevier BIOBASE SCImago Journal and Country Rank Factor
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