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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...
Atherosclerosis I: Introduction01:30

Atherosclerosis I: Introduction

Atherosclerosis is a progressive disorder characterized by the buildup of plaques on the arterial inner wall, causing them to narrow and harden over time. These plaques comprise lipids, calcium, blood components, carbohydrates, and fibrous tissue. The process primarily affects the intima of large and medium-sized arteries, reducing blood flow in any artery.Etiology and risk factorsThe cause of atherosclerosis is multifactorial, involving a complex interplay among endothelial injury, lipid...
Clot Retraction and Fibrinolysis01:16

Clot Retraction and Fibrinolysis

After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
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...
Vascular Spasm01:16

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Updated: May 26, 2026

The Arteriovenous (AV) Loop in a Small Animal Model to Study Angiogenesis and Vascularized Tissue Engineering
08:53

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Published on: November 2, 2016

Stroke, angiogenesis and phytochemicals.

Yu-Chang Chen1, Jui-Sheng Wu, Shun-Tai Yang

  • 1Institute of Neuroscience, National Yang-Ming University, Taipei, Taiwan, ROC.

Frontiers in Bioscience (Scholar Edition)
|December 29, 2011
PubMed
Summary
This summary is machine-generated.

Phytochemicals may promote new blood vessel growth after stroke, aiding neural protection and recovery. Combining phytochemicals with other therapies offers a promising approach for stroke treatment.

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08:42

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Published on: September 19, 2016

Area of Science:

  • Neuroscience
  • Cardiovascular Science
  • Pharmacology

Background:

  • Stroke is a leading cause of death and disability globally, with limited effective treatments.
  • Neuroprotective drugs have shown limited success in clinical trials for stroke patients.
  • Post-ischemic angiogenesis in the penumbra area is a key area of interest for stroke recovery.

Purpose of the Study:

  • To review current knowledge on phytochemicals and their role in post-ischemic angiogenesis.
  • To explore the potential of phytochemicals as a therapeutic strategy for stroke.
  • To discuss combinatorial treatments for stroke involving neuroprotection, angiogenesis, neurogenesis, and phytochemicals.

Main Methods:

  • Review of preclinical and clinical studies on stroke, angiogenesis, and phytochemicals.
  • Analysis of epidemiological data on phytochemical intake and stroke incidence.
  • Discussion of cellular and molecular mechanisms underlying phytochemical effects.

Main Results:

  • Phytochemicals show a reciprocal relationship with stroke incidence in epidemiological studies.
  • Angiogenesis is postulated to play a crucial role in neural protection and tissue recovery after stroke.
  • Therapeutic agents promoting angiogenesis present a promising approach for stroke treatment.

Conclusions:

  • Phytochemicals may promote post-ischemic angiogenesis, contributing to neural protection and tissue recovery.
  • Combinatorial therapeutic strategies including phytochemicals hold promise for improved stroke outcomes.
  • Further elucidation of molecular mechanisms is needed to optimize phytochemical-based stroke therapies.