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

Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...
Ischemic Stroke l: Introduction01:15

Ischemic Stroke l: Introduction

Ischemic stroke is an acute cerebrovascular condition in which blood flow to a brain region is suddenly interrupted, leading to tissue infarction. Neurons depend on continuous oxygen and glucose supply, so even brief reductions in perfusion cause energy failure, ionic imbalance, and irreversible injury. Ischemic strokes are classified into thrombotic and embolic types based on their underlying mechanisms.Thrombotic MechanismsThrombotic stroke develops when a clot forms within a cerebral artery.
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...
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...

You might also read

Related Articles

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

Sort by
Same author

Integrative CSF profiling identifies disease-specific immune responses in leptomeningeal disease.

Cell reports. Medicine·2026
Same author

Comparative cross-methodological analysis of the IDH-wildtype glioblastoma tumor microenvironment.

Journal of cancer research and clinical oncology·2026
Same author

Advancing CNS tumor diagnostics with expanded DNA methylation-based classification.

Cancer cell·2025
Same author

Spatial immune profiling defines a subset of human gliomas with functional tertiary lymphoid structures.

Immunity·2025
Same author

Glioma‑associated microglia and macrophages as a potential target for mTOR inhibition in glioblastoma.

Molecular medicine reports·2025
Same author

Outcome-associated factors in a molecularly defined cohort of central neurocytoma.

Acta neuropathologica·2025

Related Experiment Video

Updated: Jun 26, 2026

A Model for Encephalomyosynangiosis Treatment after Middle Cerebral Artery Occlusion-Induced Stroke in Mice
06:54

A Model for Encephalomyosynangiosis Treatment after Middle Cerebral Artery Occlusion-Induced Stroke in Mice

Published on: June 22, 2022

Angiogenesis after cerebral ischemia.

Heike Beck1, Karl H Plate

  • 1Institute of Cardiovascular Physiology, Walter Brendel Center of Experimental Medicine, Ludwig-Maximilians University Munich, Marchioninistr. 27, 81377, Munich, Germany. Heike.Beck@med.uni-muenchen.de

Acta Neuropathologica
|January 15, 2009
PubMed
Summary

Brain ischemia triggers new blood vessel growth (angiogenesis) to aid recovery. Understanding these mechanisms is key for developing new stroke treatments, despite potential risks from growth factors.

More Related Videos

Two-vessel Occlusion Mouse Model of Cerebral Ischemia-reperfusion
07:34

Two-vessel Occlusion Mouse Model of Cerebral Ischemia-reperfusion

Published on: March 1, 2019

Related Experiment Videos

Last Updated: Jun 26, 2026

A Model for Encephalomyosynangiosis Treatment after Middle Cerebral Artery Occlusion-Induced Stroke in Mice
06:54

A Model for Encephalomyosynangiosis Treatment after Middle Cerebral Artery Occlusion-Induced Stroke in Mice

Published on: June 22, 2022

Two-vessel Occlusion Mouse Model of Cerebral Ischemia-reperfusion
07:34

Two-vessel Occlusion Mouse Model of Cerebral Ischemia-reperfusion

Published on: March 1, 2019

Area of Science:

  • Neuroscience
  • Vascular Biology
  • Regenerative Medicine

Background:

  • The adult brain vasculature is typically stable.
  • Brain ischemia induces endothelial cell proliferation and angiogenesis, especially at the ischemic boundary zone.
  • Angiogenesis enhances oxygen and nutrient supply, supporting neurogenesis and synaptogenesis for functional recovery.

Purpose of the Study:

  • To review the molecular mechanisms of angiogenesis following cerebral ischemia.
  • To discuss therapeutic strategies for stimulating post-ischemic angiogenesis in stroke treatment.

Main Methods:

  • Literature review of molecular mechanisms of angiogenesis post-cerebral ischemia.
  • Discussion of experimental, pharmacological, and cellular approaches to enhance angiogenesis.

Main Results:

  • Cerebral ischemia activates angiogenesis, primarily in the ischemic boundary zone.
  • New blood vessels improve tissue supply and facilitate neurorestorative processes.
  • Certain growth factors involved in angiogenesis can increase vascular permeability, posing potential risks.

Conclusions:

  • Understanding the molecular basis of post-ischemic angiogenesis is crucial for stroke therapy development.
  • Targeting angiogenesis offers therapeutic potential, but careful consideration of adverse effects is necessary.
  • Experimental approaches show promise for enhancing beneficial angiogenesis after stroke.