Thyroid Hormone Receptor Antagonists; from Environmental Pollution to Novel Small Molecules

Research output: Chapter in Book/Conference proceeding with ISSN or ISBNChapter

Abstract

hyroid hormone receptors (TRs) are nuclear receptors which control transcription, and thereby have effects in all cells within the body. TRs are an important regulator in many basic physiological processes including development, growth, metabolism, and cardiac function. The hyperthyroid condition results from an over production of thyroid hormones resulting in a continual stimulation of thyroid receptors which is detrimental for the patient. Therapies for hyperthyroidism are available, but there is a need for new small molecules that act as TR antagonists to treat hyperthyroidism. Many compounds exhibit TR antagonism and are considered detrimental to health. Some drugs in the clinic (most importantly, amiodarone) and environmental pollution exhibit TR antagonist properties and thus have the potential to induce hypothyroidism in some people. This chapter provides an overview of novel small molecules that have been specifically designed or screened for their TR antagonist activity as novel treatments for hyperthyroidism. While novel compounds have been identified, to date none have been developed sufficiently to enter clinical trials. Furthermore, a discussion on other sources of TR antagonists is discussed in terms of side effects of current drugs in the clinic as well as environmental pollution.
Original languageEnglish
Title of host publicationVitamins and Hormones
EditorsGerald Litwack
Place of PublicationUK
PublisherElsevier
Pages147-162
Number of pages16
Volume106
ISBN (Print)9780128141168
DOIs
Publication statusPublished - 5 Jun 2017

Publication series

NameVitamins and Hormones

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  • Cite this

    Mackenzie, L. (2017). Thyroid Hormone Receptor Antagonists; from Environmental Pollution to Novel Small Molecules. In G. Litwack (Ed.), Vitamins and Hormones (Vol. 106, pp. 147-162). (Vitamins and Hormones). Elsevier. https://doi.org/10.1016/bs.vh.2017.04.004