Related Experiment Video
Updated: May 15, 2026

05:39
Spontaneous Murine Model of Anaplastic Thyroid Cancer
Published on: February 3, 2023
Thyroid in 2012: Advances in thyroid development, hormone action and neoplasia
1University of Cambridge, Institute of Metabolic Science, Addenbrooke's Hospital, UK. kkc1@medschl.cam.ac.uk
Nature Reviews. Endocrinology
|January 9, 2013
Summary
Researchers discovered that thyroid hormones boost autophagy and developed methods to generate functional thyroid tissue in vitro. Gene expression profiling can now distinguish benign thyroid nodules, advancing thyroid disorder research.
Area of Science:
- Endocrinology and Molecular Biology
- Thyroid Research
- Cellular Biology
Background:
- Thyroid hormones play crucial roles in cellular processes, including autophagy.
- Genetic defects affecting thyroid hormone action, such as those in Thyroid Hormone Receptor alpha (TRα), lead to specific clinical conditions.
- Understanding thyroid nodule characteristics is vital for accurate diagnosis and patient management.
Purpose of the Study:
- To summarize recent advancements in thyroid research, focusing on in vitro tissue generation, hormone signaling, and diagnostic techniques.
- To highlight the role of thyroid hormones in stimulating autophagy.
- To review findings related to TRα defects and potential therapeutic interventions like di-iodothyropropionic acid for MCT8 deficiency.
- To present the utility of gene expression profiling in identifying benign thyroid nodules.
Main Methods:
- In vitro generation of functional thyroid tissue.
- Investigation of thyroid hormone effects on autophagy.
- Identification and study of patients with TRα defects.
- Assessment of di-iodothyropropionic acid in ameliorating MCT8 deficiency.
- Application of gene expression profiling for thyroid nodule classification.
Main Results:
- Functional thyroid tissue can be successfully generated in vitro.
- Thyroid hormones were confirmed to stimulate autophagy.
- Defects in TRα were identified in patient cohorts.
- Di-iodothyropropionic acid demonstrated efficacy in ameliorating MCT8 deficiency.
- Gene expression profiling proved effective in distinguishing benign thyroid nodules.
Conclusions:
- Significant progress has been made in thyroid tissue engineering and understanding thyroid hormone action.
- Targeted therapies for specific thyroid-related genetic disorders are emerging.
- Gene expression profiling offers a promising non-invasive tool for thyroid nodule diagnosis.
Related Concept Videos
Hyperthyroidism II: Pathophysiology
Hyperthyroidism is a hypermetabolic state caused by elevated levels of thyroid hormones, triiodothyronine (T3) and thyroxine (T4). It results from dysregulation at the thyroid, pituitary, or immune system level and affects multiple organ systems.PathophysiologyThe most common cause of hyperthyroidism is Graves’ disease, an autoimmune disorder in which antibodies, specifically thyroid-stimulating antibodies (TSAb), a subtype of TSH receptor antibodies (TRAb), bind to and activate TSH receptors...
Synthesis and Regulation of Thyroid Hormones
Low blood levels of the thyroid hormones — triiodothyronine (T3) and thyroxine (T4) — signal the hypothalamus to release the thyrotropin-releasing hormone (TRH). TRH then reaches the pituitary gland and stimulates the release of thyroid-stimulating hormone(TSH) into the bloodstream.
Upon reaching the thyroid gland, TSH stimulates the follicular cells' active uptake of iodide ions from the blood. The ions diffuse to the apical surface of the cells and are oxidized to iodine. The iodine is then...
Upon reaching the thyroid gland, TSH stimulates the follicular cells' active uptake of iodide ions from the blood. The ions diffuse to the apical surface of the cells and are oxidized to iodine. The iodine is then...
Hypothyroidism II: Pathophysiology
Hypothyroidism is a disorder characterized by insufficient production of thyroid hormones, which regulate metabolism, energy balance, and multiple organ systems.TypesHypothyroidism is classified based on the level of dysfunction. Primary hypothyroidism results from intrinsic thyroid gland dysfunction, causing reduced hormone production despite normal or increased stimulation. Secondary hypothyroidism arises from inadequate thyroid-stimulating hormone (TSH) secretion by the pituitary. Tertiary...
Graves Disease II: Pathophysiology
Graves’ disease is an autoimmune disorder characterized by the production of thyroid-stimulating immunoglobulins (TSI) that activate TSH receptors, leading to excessive synthesis and release of thyroid hormones (T3 and T4) and resulting in hyperthyroidism.Among all causes of hyperthyroidism, Graves’ disease is the most common and can happen at any age, though it is more frequent in women. It produces a hypermetabolic state with features such as weight loss, tachycardia, tremor, and heat...
Functions of Thyroid Hormones
The thyroid hormone (TH) plays a pivotal role in the intricate orchestration of physiological processes, exerting profound effects on development, metabolism, and homeostasis throughout different life stages.
TH is indispensable for the normal development and maturation of the skeletal, muscular, and nervous systems during fetal and childhood growth. It facilitates bone mineral turnover and regulates protein synthesis in developing tissues, contributing significantly to overall growth and...
TH is indispensable for the normal development and maturation of the skeletal, muscular, and nervous systems during fetal and childhood growth. It facilitates bone mineral turnover and regulates protein synthesis in developing tissues, contributing significantly to overall growth and...
Hyperthyroidism I: Introduction
Hyperthyroidism is a type of thyrotoxicosis characterized by the thyroid gland's overproduction of the thyroid hormones triiodothyronine (T3) and thyroxine (T4). This hormone excess increases the basal metabolic rate and enhances sensitivity to catecholamines.DiagnosisDiagnosis is based on clinical features and biochemical testing. It typically shows suppressed thyroid-stimulating hormone (TSH) levels below 0.4 mIU/L, with elevated free T3 and/or T4. Additional tests, including thyroid...
