Cellular and Molecular Basis of Deiodinase-Regulated Thyroid Hormone Signaling

Gereben, B [Gereben, Balázs (Pajzsmirigy endok...), szerző] Molekuláris Sejt Metabolizmus Kutatócsoport (KOKI / ENO); Zavacki, AM; Ribich, S; Kim, BW; Huang, SA; Simonides, WS; Zeold, A [Zeöld, Anikó (Sejtbiológia), szerző] Endokrin Neurobiológiai Kutatócsoport (KOKI / ENO); Bianco, AC

Angol nyelvű Tudományos Összefoglaló cikk (Folyóiratcikk)
Megjelent: ENDOCRINE REVIEWS 0163-769X 1945-7189 29 (7) pp. 898-938 2008
  • SJR Scopus - Endocrinology: D1
    The iodothyronine deiodinases initiate or terminate thyroid hormone action, and therefore are critical for the biological effects mediated by thyroid hormone. Over the years research has focused on their role in preserving serum levels of the biologically active molecule triiodothyronine (T3) during iodine deficiency. More recently, a fascinating new role of these enzymes has been unveiled. The activating deiodinase (D2) and the inactivating deiodinase (D3) can locally increase or decrease thyroid hormone signaling in a tissue- and temporal-specific fashion, independently of changes in thyroid hormone serum concentrations. This mechanism is particularly relevant as deiodinase expression can be modulated by a wide variety of endogenous signaling molecules such as sonic hedgehog, NF-kappaB, growth factors, bile acids, HIF-1alpha, as well as a growing number of xenobiotic substances. In light of these findings, it seems clear that deiodinases play a much broader role than once thought, with great ramifications for the control of thyroid hormone signaling during vertebrate development and metamorphosis, as well as injury response, tissue repair, hypothalamic function, and energy homeostasis in adults.
    Hivatkozás stílusok: IEEEACMAPAChicagoHarvardCSLMásolásNyomtatás
    2021-08-03 08:59