Abstract
Accumulating evidence has shown that thyroid hormones (THs) are vital for female reproductive system homeostasis. THs regulate the reproductive functions through thyroid hormone receptors (THRs)-mediated genomic- and integrin-receptor-associated nongenomic mechanisms, depending on TH ligand status and DNA level, as well as transcription and extra-nuclear signaling transduction activities. These processes involve the binding of THs to intracellular THRs and steroid hormone receptors or membrane receptors and the recruitment of hormone-response elements. In addition, THs and other reproductive hormones can activate common signaling pathways due to their structural similarity and shared DNA consensus sequences among thyroid, peptide, and protein hormones and their receptors, thus constituting a complex and reciprocal interaction network. Moreover, THs not only indirectly affect the synthesis, secretion, and action of reproductive hormones, but are also regulated by these hormones at the same time. This crosstalk may be one of the pivotal factors regulating female reproductive behavior and hormone-related diseases, including tumors. Elucidating the interaction mechanism among the aforementioned hormones will contribute to apprehending the etiology of female reproductive diseases, shedding new light on the treatment of gynecological disorders.
Highlights
Academic Editor: Paolo ChieffiThe butterfly-shaped thyroid gland is an endocrine organ located below the thyroid cartilage in the mammalian neck [1,2]
thyroid-hormone response element (TRE) is recognized by the members of the superfamilies and accumulates near the target gene promoter to activate or inhibit transcription [26,29]; the ability of TRE to respond to other steroid hormone receptors enables the crosstalk between thyroid hormone receptors (THRs) and steroid hormone receptors, providing multiple selectivity for gene regulation
The other way of thyroid hormones (THs) influence the female reproductive system is via nongenomic effects, in which THs stimulate the mitochondria and cytoskeleton in the cytoplasm or integrin receptors on the cell membrane to target extra-nuclear signaling regulated by hormone-mediated rapid cellular response without involving the intra-nuclear THRs induced genomic effects by T3 [19,103,104]
Summary
The butterfly-shaped thyroid gland is an endocrine organ located below the thyroid cartilage in the mammalian neck [1,2]. The thyroid gland is responsible for secreting thyroid hormones (THs), including triiodothyronine (T3) and thyroxine (T4), both of which are mainly generated by thyroid follicular epithelial cells [3]. The synthesis and secretion of THs are regulated by thyroid-stimulating hormone (TSH) released by the pituitary gland [4]. T4 accounts for approximately 80% of the total THs, whereas T3 only accounts for about. THs are negatively feedback regulated by TSH and thyrotropin-releasing hormone (TRH) to maintain normal TH levels in the blood [8,9]. After entering into the blood, THs are rapidly transported to target tissues, where they facilitate the body’s utilization of energy and support the functions of vital organs, including maintaining the normal function of the reproductive system. Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations.
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