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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...
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...
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.
Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
Transient Ischemic Attack l: Introduction01:26

Transient Ischemic Attack l: Introduction

A transient ischemic attack (TIA) is a brief episode of neurological dysfunction caused by a temporary, focal reduction in cerebral blood flow. Although symptoms resemble those of an ischemic stroke, the interruption in perfusion is short-lived and does not cause permanent infarction. TIAs are clinically important because they often serve as early warning events for future stroke.Mechanisms of Transient Cerebral IschemiaTransient cerebral ischemia may arise through several mechanisms. One...

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Related Experiment Video

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 and Ischemic Stroke.

Gongda Li1, Zhongyu Liu1, Wenwen Li1

  • 1Institute of Traditional Chinese Medicine, Heilongjiang University of Chinese Medicine, 24 Heping Road, Harbin, 150040, China.

Current Neurovascular Research
|June 8, 2026

View abstract on PubMed

Summary
This summary is machine-generated.

Promoting angiogenesis is crucial for treating ischemic stroke by restoring blood flow and aiding recovery. Further research is needed to understand the causal mechanisms of signaling pathways involved in post-stroke angiogenesis for better therapeutic strategies.

Keywords:
Ischemic strokeangiogenesisbrain injuriessignaling pathwaysstem cellssystematic literature.

More Related Videos

Assessment of Vascular Regeneration in the CNS Using the Mouse Retina
07:32

Assessment of Vascular Regeneration in the CNS Using the Mouse Retina

Published on: June 23, 2014

Related Experiment Videos

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

Assessment of Vascular Regeneration in the CNS Using the Mouse Retina
07:32

Assessment of Vascular Regeneration in the CNS Using the Mouse Retina

Published on: June 23, 2014

Area of Science:

  • Neuroscience
  • Cardiovascular Research
  • Regenerative Medicine

Background:

  • Stroke remains a leading global cause of death and disability.
  • The health burden associated with stroke has increased significantly in recent decades.
  • Understanding post-stroke recovery mechanisms is critical.

Purpose of the Study:

  • To systematically review cell types and signaling pathways modulating angiogenesis after cerebral ischemia.
  • To emphasize the need for therapeutic strategies targeting angiogenic mechanisms in ischemic stroke.
  • To bridge the gap between preclinical findings and clinical applications.

Main Methods:

  • Systematic literature search of PubMed, Google Scholar, and Web of Science (2020-2025).
  • Keywords: "cerebral ischemia" and "angiogenesis".
  • Prioritized clinical trials, supplemented with animal studies when necessary.
  • Main Results:

    • Angiogenesis is vital for stroke recovery, restoring blood flow and promoting neural regeneration.
    • Key cell types (e.g., bone marrow-derived cells) and signaling pathways (e.g., PI3K/AKT, JAK2/STAT3, HIF-1α/VEGF) are implicated.
    • Current evidence shows correlation, not definitive causation, for these pathways.

    Conclusions:

    • Preclinical studies suggest regulatory roles for signaling pathways in post-ischemic angiogenesis.
    • Establishing clear causal mechanisms requires more rigorous mechanistic and clinical translational studies.
    • Targeting angiogenesis offers a promising therapeutic avenue for ischemic stroke, addressing unmet clinical needs.