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Related Concept Videos

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...
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...
Overview of Cell-Matrix Interactions01:24

Overview of Cell-Matrix Interactions

The extracellular matrix or ECM holds cells together to form a tissue and allows the cells within the tissue to communicate. ECM comprises proteins such as fibronectin, collagen, laminin, etc. The most abundant protein in this space is collagen. Collagen fibers are interwoven with carbohydrate-containing protein molecules called proteoglycans. ECM allows cell migration and provides a structural scaffold at cell adhesion that anchors the cell when the extracellular matrix proteins interact with...
Chronic Inflammation: Introduction01:12

Chronic Inflammation: Introduction

Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...

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Related Experiment Video

Updated: Jun 23, 2026

An Immunohistopathologic Study to Profile the Folate Receptor Beta Macrophage and Vascular Immune Microenvironment in Giant Cell Arteritis
06:35

An Immunohistopathologic Study to Profile the Folate Receptor Beta Macrophage and Vascular Immune Microenvironment in Giant Cell Arteritis

Published on: February 8, 2019

Giant cell arteritis and angiogenesis: a review.

Ellen Browne Mitchell1, Dean M Cestari

  • 1Massachusetts Eye and Ear Infirmary, 243 Charles St., Boston, MA 02114, USA. elbrowne@gmail.com

Seminars in Ophthalmology
|May 14, 2009
PubMed
Summary

Giant cell arteritis can cause vision loss through arteritic anterior ischemic optic neuropathy. This condition results from artery narrowing due to inflammation and cell growth, driven by inflammatory factors.

Area of Science:

  • Vascular Inflammation
  • Ophthalmology
  • Pathology

Background:

  • Giant cell arteritis (GCA) is a large and medium-sized artery vasculitis.
  • Arteritic anterior ischemic optic neuropathy (AAION) is the most frequent cause of vision loss in GCA.
  • AAION-related ischemia is thought to stem from intimal hyperplasia-induced luminal stenosis.

Purpose of the Study:

  • To investigate the underlying mechanisms of ischemia in arteritic anterior ischemic optic neuropathy.
  • To identify key factors contributing to the development of intimal hyperplasia in GCA.

Main Methods:

  • Review of existing literature on GCA and AAION.
  • Analysis of pathological findings in affected arteries.
  • Examination of inflammatory and pro-angiogenic pathways involved.

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Investigating Angiogenesis on a Functional and Molecular Level by Leveraging the Scratch Wound Migration Assay and the Spheroid Sprouting Assay
09:16

Investigating Angiogenesis on a Functional and Molecular Level by Leveraging the Scratch Wound Migration Assay and the Spheroid Sprouting Assay

Published on: May 31, 2024

Related Experiment Videos

Last Updated: Jun 23, 2026

An Immunohistopathologic Study to Profile the Folate Receptor Beta Macrophage and Vascular Immune Microenvironment in Giant Cell Arteritis
06:35

An Immunohistopathologic Study to Profile the Folate Receptor Beta Macrophage and Vascular Immune Microenvironment in Giant Cell Arteritis

Published on: February 8, 2019

Modified In Vivo Matrix Gel Plug Assay for Angiogenesis Studies
09:03

Modified In Vivo Matrix Gel Plug Assay for Angiogenesis Studies

Published on: June 30, 2023

Investigating Angiogenesis on a Functional and Molecular Level by Leveraging the Scratch Wound Migration Assay and the Spheroid Sprouting Assay
09:16

Investigating Angiogenesis on a Functional and Molecular Level by Leveraging the Scratch Wound Migration Assay and the Spheroid Sprouting Assay

Published on: May 31, 2024

Main Results:

  • Intimal hyperplasia is a primary driver of luminal stenosis in AAION.
  • Inflammatory mediators and pro-angiogenic factors initiate and promote this process.
  • Understanding these factors is crucial for developing targeted therapies.

Conclusions:

  • AAION pathogenesis in GCA involves complex inflammatory and angiogenic signaling.
  • Targeting intimal hyperplasia and its initiators may prevent vision loss.
  • Further research into these pathways is warranted for effective GCA management.