Abstract
The thyroid hormone receptors are the mediators of a multitude of actions by the thyroid hormones in cells. Most thyroid hormone activities require interaction with nuclear receptors to bind DNA and regulate the expression of target genes. In addition to genomic regulation, thyroid hormones function via activation of specific cytosolic pathways, bypassing interaction with nuclear DNA. In the present work, we reviewed the most recent literature on the characteristics and roles of different factors involved in thyroid hormone function in particular, we discuss the genomic activity of thyroid hormone receptors in the nucleus and the functions of different thyroid hormone receptor isoforms in the cytosol. Furthermore, we describe the integrin αvβ3-mediated thyroid hormone signaling pathway and its rapid nongenomic action in the cell. We furthermore reviewed the thyroid hormone transporters enabling the uptake of thyroid hormones in the cell, and we also include a paragraph on the proteins that mediate thyroid receptors’ shuttling from the nucleus to the cytosol.
Highlights
Thyroid hormones (THs) are important regulatory molecules in the human body that mediate many metabolic and developmental processes [1,2,3,4]
The biological activities of T3 via transcriptional regulation are mediated by thyroid hormone receptors (TRs) which are encoded by two different genes, called THRA and THRB, and in humans are located on chromosomes 17 and 3, respectively [11]
Direct interaction of T3 with target genes is mediated by nuclear thyroid hormone receptors (TRs), which bind to specific sequences called thyroid response elements (TREs)
Summary
Thyroid hormones (THs) are important regulatory molecules in the human body that mediate many metabolic and developmental processes (e.g., increased basal metabolic rate, lipolysis/lipogenesis, adaptive thermogenesis, etc.) [1,2,3,4]. THs may act through alternative pathways devoid of interaction with nuclear receptors, leading to a more rapid TH action after binding to plasma membrane or cytoplasmic sites. TH action is generally defined as genomic when it directly involves interaction of the hormone with the nuclear receptor, and nongenomic when TH action is not initiated by interaction with specific nuclear receptors The latter distinction has recently been found to be overly simplistic and misleading since it seems to suggest that the nongenomic pathways lack involvement in the regulation of gene expression [6]. The aim of this review is to discuss the principal factors regulating TH effects in the cell both at the nuclear level, where a direct interaction of thyroid hormone receptors (TRs) and the DNA target occurs, and in the cytosol, where TR isoforms are involved, at least in part, in rapid nongenomic responses. The integrin αvβ3-mediated effects of TH on specific metabolic pathways are discussed
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