IMR Press / FBL / Volume 12 / Issue 4 / DOI: 10.2741/2140

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article
Thyroid hormone calorigenesis and mitochondrial redox signaling: upregulation of gene expression
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1 Molecular and Clinical Pharmacology Program, Institute of Biomedical Sciences, Faculty of Medicine, University of Chile, Santiago, Chile
2 Cellular and Molecular Biology Program, Institute of Biomedical Sciences, Faculty of Medicine, University of Chile, Santiago, Chile
Academic Editors:Alberto Boveris, Ana Navarro
Front. Biosci. (Landmark Ed) 2007, 12(4), 1220–1228; https://doi.org/10.2741/2140
Published: 1 January 2007
(This article belongs to the Special Issue Mitochondria: physiological function, signaling and oxidative damage)
Abstract

Thyroid hormone (TH, T3) is required for the normal function of most tissues, with major effects on O2 consumption and metabolic rate. These are due to transcriptional activation of respiratory genes through the interaction of T3-liganded TH receptors with TH response elements or the activation of intermediate factors, with the consequent higher rates of mitochondrial oxidative phosphorylation and reactive O2 species (ROS) generation and antioxidant depletion. The genomic effects of TH are accompanied by redox upregulation of the liver expression of cytokines (tumor necrosis factor-alpha [TNF-alpha]), enzymes (manganese superoxide dismutase), and anti-apoptotic proteins (Bcl-2), via a cascade initiated by TNF-alpha produced by Kupffer cells and involving inhibitor of kappa-B phosphorylation and nuclear factor-kappa-B activation. Thus, TH calorigenesis triggers non-genomic effects leading to an expression pattern that may represent an adaptive mechanism to re-establish redox homeostasis and promote cell survival under conditions of ROS toxicity secondary to TH-induced oxidative stress. Mechanisms of expression of respiratory and redox-sensitive genes may be functionally integrated, which could be of importance to understand the complexities of TH action and the outcome of thyroid gland dysfunction.

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