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Related Concept Videos

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...
Graves' Disease I: Introduction01:28

Graves' Disease I: Introduction

Graves' disease is an autoimmune disorder that causes hyperthyroidism, or overactivity of the thyroid gland. It results from autoantibodies called thyroid-stimulating immunoglobulins (TSIs), which bind to thyroid-stimulating hormone (TSH) receptors, leading to overstimulation of hormone production and a hypermetabolic state.EtiologyAlthough considered idiopathic, Graves’ disease has well-established contributing factors. There is a strong genetic component, with increased prevalence in...
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...
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...
Goiter01:27

Goiter

Goiter refers to an abnormal enlargement of the thyroid gland that may appear as a diffuse goiter (uniform enlargement) or nodular (single or multiple nodules). Functionally, it is classified as nontoxic (normal/low hormone levels) or toxic (excess hormone production).PathophysiologyDiffuse thyroid enlargement typically results from prolonged stimulation by thyroid-stimulating hormone (TSH) or TSH-like agents, commonly seen in hypothyroidism or iodine deficiency. In contrast, in hyperthyroid...
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...

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Related Experiment Video

Updated: Jun 28, 2026

An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma
07:01

An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma

Published on: April 17, 2013

Apoptotic study in Graves disease treated with thyroid arterial embolization.

Wei Zhao1, Bu Lang Gao, Gen Fa Yi

  • 1Medical Imaging Center, First Affiliated Hospital, Kunming Medical College, Kunmin, Yunnan Province, China.

Endocrine Journal
|November 15, 2008
PubMed
Summary

Thyroid arterial embolization effectively boosts pro-apoptotic gene expression in Graves disease (GD) thyroids. This promotes apoptosis, aiding in restoring normal thyroid size and function.

Related Experiment Videos

Last Updated: Jun 28, 2026

An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma
07:01

An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma

Published on: April 17, 2013

Area of Science:

  • Endocrinology
  • Oncology
  • Immunology

Background:

  • Graves disease (GD) is an autoimmune disorder characterized by thyroid overactivity.
  • Thyroid arterial embolization is an emerging treatment modality for GD.
  • Understanding the molecular mechanisms of GD treatment is crucial for optimizing patient outcomes.

Purpose of the Study:

  • To investigate the induction of apoptosis in the thyroid gland of patients with Graves disease following thyroid arterial embolization.
  • To evaluate the expression of key apoptosis-related genes after the procedure.

Main Methods:

  • Forty-one GD patients underwent thyroid arterial embolization.
  • Thyroid autoantibodies (TSAb, TGAb, TMAb) were measured pre- and post-embolization.
  • Thyroid biopsies were analyzed using immunohistochemistry for pro-apoptotic gene expression (Fas, FasL, Bax, Bcl-2, P53).

Main Results:

  • Before embolization, positive staining for Fas, FasL, and Bax was observed, with no P53 expression.
  • Following embolization, a significant increase in the positive cell number and staining intensity for Fas, FasL, and Bax was noted.
  • The expression of pro-apoptotic genes was enhanced post-embolization.

Conclusions:

  • Thyroid arterial embolization effectively upregulates pro-apoptotic gene expression (Fas, FasL, Bax, Bcl-2, P53) in Graves disease thyroid tissue.
  • This enhanced gene expression promotes apoptosis in GD thyroid cells.
  • The procedure aids in restoring normal thyroid size and function in GD patients.