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Related Concept Videos

Hyperthyroidism II: Pathophysiology01:27

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...
Graves Disease II: Pathophysiology01:24

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...
The Thyroid Gland01:23

The Thyroid Gland

The thyroid gland is a small, butterfly-shaped gland located in the neck and covers the anterior surface of the trachea. The gland has two lateral lobes connected by a thin tissue mass called the isthmus. Internally, each lobe comprises many small spherical structures known as thyroid follicles, surrounded by a network of blood vessels.
The follicles have a central cavity lined by simple cuboidal to squamous epithelial cells called follicular cells. These cells produce the glycoprotein...
Synthesis and Regulation of Thyroid Hormones01:20

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...
Hypothyroidism II: Pathophysiology01:23

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...
Hyperthyroidism I: Introduction01:25

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...

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Related Experiment Video

Updated: May 23, 2026

An Ex vivo Culture System to Study Thyroid Development
08:33

An Ex vivo Culture System to Study Thyroid Development

Published on: June 6, 2014

Thyroid regeneration: characterization of clear cells after partial thyroidectomy.

Takashi Ozaki1, Tsutomu Matsubara, Daekwan Seo

  • 1Laboratory of Metabolism, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.

Endocrinology
|March 29, 2012
PubMed
Summary

Partial thyroidectomy in rats induced thyroid regeneration. Immature clear cells, potentially derived from stem cells or altered C/follicular cells, emerged and may aid in thyroid repair.

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Published on: September 15, 2023

Area of Science:

  • Endocrinology
  • Cell Biology
  • Regenerative Medicine

Background:

  • The thyroid gland is not traditionally considered regenerative.
  • Thyroid growth can occur in response to pituitary-thyroid axis perturbations.
  • Partial thyroidectomy (PTx) was employed to investigate thyroid regeneration potential.

Purpose of the Study:

  • To explore the regenerative capacity of the thyroid gland following partial thyroidectomy.
  • To identify cellular and molecular changes indicative of thyroid repair and regeneration.
  • To investigate the origin and characteristics of cells involved in thyroid regrowth.

Main Methods:

  • Partial thyroidectomy (PTx) in a rodent model.
  • Bromodeoxyuridine (BrdU) labeling to track cell proliferation.
  • Electron microscopy for cellular ultrastructure analysis.
  • Gene expression profiling using microarray and pathway analysis.
  • Measurement of serum Thyroid-Stimulating Hormone (TSH) levels.

Main Results:

  • Increased proliferation (BrdU-positive cells) observed in central thyroid areas post-PTx.
  • Appearance of 'clear cells' with characteristics of both C cells and follicular cells.
  • Some proliferating cells expressed Foxa2, a definitive endoderm marker.
  • PTx induced significant changes in serum TSH and T4 levels, creating a goitrogenic environment.
  • Gene expression analysis revealed alterations in pathways related to embryonic development and cancer.

Conclusions:

  • Thyroid regeneration after PTx involves the proliferation of existing cells and potentially stem/progenitor cells.
  • Both C cells and follicular cells may dedifferentiate into immature 'clear cells'.
  • These immature clear cells are implicated in the thyroid gland's repair and regenerative processes.
  • The study challenges the notion of the thyroid as a non-regenerative organ.