Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...
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...
Functions of Thyroid Hormones01:18

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...
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...
Mechanism of Angiogenesis01:10

Mechanism of Angiogenesis

Blood vessel formation starts early during embryonic development, around day 7. In the extraembryonic yolk sac, mesodermal precursor cells called hemangioblast proliferate and differentiate into angioblast. Angioblasts express vascular endothelial growth factor receptor 2 or VEGFR2, which binds VEGF-A, a proangiogenic factor, guiding blood vessel formation. VEGF signaling promotes angioblasts to form a blood island in the developing embryo. Angioblasts further differentiate, giving rise to...
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...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Thyroid hormones, mitochondria, aging, and cancer.

Frontiers in endocrinology·2026
Same author

Additional considerations in cancer cell radioresistance, integrin αvβ3 and thyroid hormones.

Endocrine research·2024
Same author

Editorial Expression of Concern: Response of human pancreatic cancer cell xenografts to tetraiodothyroacetic acid nanoparticles.

Discover oncology·2023
Same author

Retraction notice to "Thyroid hormone is a MAPK-dependent growth factor for thyroid cancer cells and is anti-apoptotic" [Steroids 72(2) 2007 180-187].

Steroids·2023
Same author

What is thyroid function in your just-diagnosed cancer patient?

Frontiers in endocrinology·2023
Same author

(Thyroid) Hormonal regulation of breast cancer cells.

Frontiers in endocrinology·2023
Same journal

Cardiovascular Risk Assessment: A Review of Current Models and Emerging Determinants, including Biomarkers, Genetics, and Artificial Intelligence.

Current cardiology reviews·2026
Same journal

Decoding the Genetic Architecture of Acute Coronary Syndrome: A Review on Integrated Medical Modeling.

Current cardiology reviews·2026
Same journal

Prognostic Value of Ceramide-Based Lipid Scores in Cardiovascular Disease and Heart Failure: Insights From CERT1, CERT2, and Ceramide Ratios.

Current cardiology reviews·2026
Same journal

Sudden Arrhythmic Death Presenting with Convulsive Syncope In A Young Man With Severe Coronary Atherosclerosis And Hyperthyroidism: A Case Report.

Current cardiology reviews·2026
Same journal

Bridging Dermatology and Cardiology: The Link between Skin Lesions and Cardiovascular Risk.

Current cardiology reviews·2026
Same journal

A Comprehensive Review on Thoracic Fluid Measurement Devices.

Current cardiology reviews·2026
See all related articles

Related Experiment Video

Updated: Jun 17, 2026

An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma
07:01

An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma

Published on: April 17, 2013

Thyroid hormone-induced angiogenesis.

Paul J Davis1, Faith B Davis, Shaker A Mousa

  • 1Ordway Research Institute, Inc., Albany, New York.

Current Cardiology Reviews
|January 13, 2010
PubMed
Summary
This summary is machine-generated.

Thyroid hormones like thyroxine (T4) and triiodothyronine (T3) promote new blood vessel growth (angiogenesis) by signaling through cell surface integrins. This process supports blood vessel density and can aid healing in ischemic tissues.

More Related Videos

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
07:02

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

Published on: August 23, 2019

Related Experiment Videos

Last Updated: Jun 17, 2026

An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma
07:01

An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma

Published on: April 17, 2013

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
07:02

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

Published on: August 23, 2019

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Cardiovascular Research

Background:

  • Thyroid hormone analogues, including L-thyroxine (T4), 3,5,3-triiodo-L-thyronine (T3), and diiodothyropropionic acid (DITPA), have demonstrated pro-angiogenic activity.
  • Previous research indicates that thyroid hormone-induced neovascularization is initiated at a cell surface receptor, specifically an integrin.

Purpose of the Study:

  • To elucidate the mechanism of thyroid hormone-induced angiogenesis.
  • To investigate the role of intracellular signaling pathways and growth factor secretion in thyroid hormone-mediated vascularization.

Main Methods:

  • Utilized model systems of angiogenesis to study thyroid hormone effects.
  • Employed intracellular signaling analysis, focusing on extracellular regulated kinase 1/2 (ERK1/2).
  • Assessed the secretion of vascular growth factors, such as basic fibroblast growth factor (bFGF).
  • Conducted intact animal studies to evaluate endogenous thyroid hormone effects on blood vessel density and therapeutic potential in ischemic conditions.

Main Results:

  • Thyroid hormone signaling is transduced intracellularly via ERK1/2.
  • This signaling cascade leads to the secretion of bFGF and other vascular growth factors, promoting angiogenesis.
  • Endogenous thyroid hormone supports blood vessel density in critical organs like the heart and brain.
  • Administration of thyroid hormone effectively induces angiogenesis in animal models of ischemic limbs.

Conclusions:

  • Thyroid hormones play a significant role in regulating angiogenesis through a cell surface receptor-mediated pathway.
  • The ERK1/2 signaling pathway is crucial for mediating the pro-angiogenic effects of thyroid hormones.
  • Thyroid hormone administration represents a potential therapeutic strategy for promoting vascularization in ischemic diseases.