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 T(3) 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, independent of changes in thyroid hormone serum concentrations. This mechanism is particularly relevant because deiodinase expression can be modulated by a wide variety of endogenous signaling molecules such as sonic hedgehog, nuclear factor-kappaB, growth factors, bile acids, hypoxia-inducible factor-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.

中文翻译：

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脱碘酶调节甲状腺激素信号传导的细胞和分子基础。

碘甲状腺原氨酸脱碘酶启动或终止甲状腺激素作用，因此对于甲状腺激素介导的生物效应至关重要。多年来，研究重点关注它们在碘缺乏期间维持生物活性分子 T(3) 血清水平的作用。最近，这些酶的一个令人着迷的新作用被揭示。活化脱碘酶 (D2) 和失活脱碘酶 (D3) 可以以组织和时间特异性方式局部增加或减少甲状腺激素信号传导，与甲状腺激素血清浓度的变化无关。这种机制特别相关，因为脱碘酶的表达可以通过多种内源信号分子调节，例如音刺猬、核因子-κB、生长因子、胆汁酸、缺氧诱导因子-1α以及越来越多的异生素物质。根据这些发现，脱碘酶的作用似乎比以前想象的要广泛得多，它对脊椎动物发育和变态过程中甲状腺激素信号的控制以及损伤反应、组织修复、下丘脑功能和能量产生巨大影响。成人的体内平衡。