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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...
Overview of Exosomes01:36

Overview of Exosomes

Exosomes are stable, lipid bilayer-enclosed vesicles capable of crossing biological barriers. They can carry a wide range of molecules required for intercellular communication. Once exosomes are released from the cell where they originated, they enter a recipient cell through various pathways such as fusion, receptor-mediated endocytosis, macropinocytosis, and phagocytosis.
Stahl et al. discovered exosomes in 1983, but the exosomes were initially considered waste products released from the...
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...
Cytotoxic Edema: Pathophysiology01:21

Cytotoxic Edema: Pathophysiology

Cytotoxic edema is a form of cerebral edema characterized by intracellular swelling of neurons, astrocytes, and other glial cells. It develops when the mechanisms responsible for maintaining ionic gradients across the cell membrane become impaired. Under normal physiological conditions, the sodium–potassium ATPase actively transports sodium ions out of the cell and potassium ions into the cell, preserving osmotic balance and enabling electrical signaling. This pump requires a continuous supply...
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 29, 2026

Extraction of Extracellular Vesicles from Whole Tissue
09:03

Extraction of Extracellular Vesicles from Whole Tissue

Published on: February 7, 2019

Plasma-derived exosomes from Graves' orbitopathy: Pathogenic entities causing tissue lesions.

Zhihui Xu1, Xiaoli Bao1, Xi Wang1

  • 1State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, No.54 Xianlie Road, Yuexiu District, Guangzhou, Guangdong Province, 510060, China.

Experimental Eye Research
|May 27, 2026
PubMed
Summary

Circulating exosomes from Graves' orbitopathy (GO) patients promote disease progression by reprogramming orbital cells. Inhibiting miR-221-5p offers a potential therapeutic strategy for this autoimmune eye condition.

Keywords:
AMPKAnimal modelExosomeGraves' orbitopathySingle-cell RNA sequencingmiRNA

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Last Updated: May 29, 2026

Extraction of Extracellular Vesicles from Whole Tissue
09:03

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Published on: February 7, 2019

Labeling of Extracellular Vesicles for Monitoring Migration and Uptake in Cartilage Explants
07:58

Labeling of Extracellular Vesicles for Monitoring Migration and Uptake in Cartilage Explants

Published on: October 4, 2021

Area of Science:

  • Immunology
  • Ophthalmology
  • Cell Biology

Background:

  • Graves' orbitopathy (GO) is an autoimmune disorder causing orbital inflammation, fibrosis, and adipogenesis.
  • Circulating exosomes are key intercellular communicators implicated in autoimmune diseases.
  • The specific role of exosomes in GO pathogenesis and disease progression remains unclear.

Purpose of the Study:

  • To investigate the pathogenic role of circulating exosomes in Graves' orbitopathy.
  • To elucidate the mechanisms by which exosomes drive systemic-to-local disease progression in GO.
  • To identify potential therapeutic targets within exosome-mediated pathways.

Main Methods:

  • Isolated and characterized exosomes from GO patients (GO-Exos) and healthy controls.
  • Assessed exosome effects on human orbital fibroblasts in vitro.
  • Developed a murine model of GO using GO-Exos administration.
  • Evaluated disease progression via clinical, histopathological, imaging, and single-cell RNA sequencing analyses.
  • Investigated the role of miR-221-5p and the CACNG4/AMPK pathway.

Main Results:

  • GO-Exos induced proinflammatory, profibrotic, and adipogenic phenotypes in orbital fibroblasts, upregulating IGF-1R and TSHR.
  • In vivo administration of GO-Exos recapitulated GO hallmarks in mice, including thyroid dysfunction and orbital changes.
  • miR-221-5p was identified as a key mediator of orbital remodeling by suppressing CACNG4/AMPK.
  • Single-cell RNA sequencing revealed exosome-driven cellular reprogramming, including altered immune cell populations.

Conclusions:

  • Circulating exosomes are novel pathogenic drivers in Graves' orbitopathy.
  • Exosomes mediate immunopathogenesis in autoimmune orbitopathies through mechanisms like miR-221-5p.
  • These findings provide a basis for understanding exosome-driven autoimmunity in GO and related conditions.