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Related Concept Videos

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...
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
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...
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...
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...
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: May 24, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

Riedel's thyroiditis - a case report with genes' expression studies.

Katarzyna Wojciechowska-Durczyńska1, Adam Durczyński, Stanisław Sporny

  • 1Department of Endocrinology and Metabolic Diseases, Polish Mother's Memorial Hospital Research Institute, Medical University of Lodz, Rzgowska St, No, 281/289, 93-338 Lodz, Poland. alewin@csk.umed.lodz.pl.

Thyroid Research
|March 9, 2012
PubMed
Summary
This summary is machine-generated.

Genetic studies in Riedel's thyroiditis reveal altered expression of PIK3CA and CDH3 genes. This may suggest a molecular link between this rare thyroid condition and certain cancers, warranting further investigation.

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Last Updated: May 24, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

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

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Oncology

Background:

  • Riedel's thyroiditis is a rare, fibrosing thyroid condition with an unknown genetic basis.
  • This study investigates gene expression profiles in patients with Riedel's thyroiditis.

Purpose of the Study:

  • To explore the genetic background of Riedel's thyroiditis by analyzing gene expression levels.
  • To identify potential molecular pathways associated with the disease.

Main Methods:

  • Quantitative real-time PCR was used to assess the expression of 10 specific genes (PIK3CA, PIK3CD, PIK3CG, Tg, TGFB1, THRB, COL1, CDKN1C, CDH3, and CACNA2D2) in thyroid specimens.
  • Gene expression levels were compared between Riedel's thyroiditis cases and control thyroid tissues.

Main Results:

  • Increased expression of PIK3CA and CDH3 genes was observed in a subset of Riedel's thyroiditis cases compared to controls.
  • The remaining genes showed comparable or lower expression levels in the affected tissues.

Conclusions:

  • The findings suggest a potential association between elevated PIK3CA and CDH3 gene expression and Riedel's thyroiditis.
  • This molecular alteration may indicate a possible link to neoplastic processes, requiring further genetic research.
  • Challenges in gene expression studies for Riedel's thyroiditis include tissue fibrosis leading to limited genetic material.