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Related Experiment Video

Updated: May 22, 2026

Embryonic Stem Cell-Derived Endothelial Cells for Treatment of Hindlimb Ischemia
09:11

Embryonic Stem Cell-Derived Endothelial Cells for Treatment of Hindlimb Ischemia

Published on: January 23, 2009

CD36 as a therapeutic target for endothelial dysfunction in stroke.

Sunghee Cho1

  • 1Department of Neurology/ Neuroscience, Weill Cornell Medical College at Burke Medical Research Institute, 785 Mamaroneck Ave., White Plains, New York 10605, USA. suc2002@med.cornell.edu

Current Pharmaceutical Design
|May 12, 2012
PubMed
Summary

Stroke involves multiple harmful pathways. Targeting the CD36 receptor and its ligands may offer new therapeutic strategies for stroke by addressing inflammation and endothelial dysfunction.

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Area of Science:

  • Neuroscience
  • Immunology
  • Cardiovascular Biology

Background:

  • Stroke pathology is complex, involving inflammation, oxidative stress, and cell death pathways.
  • Single-pathway interventions have limited success in human stroke due to its multifactorial nature.
  • CD36, a scavenger receptor, plays a role in both normal physiology and pathological conditions.

Purpose of the Study:

  • To review CD36-ligand interactions relevant to endothelial function.
  • To explore the therapeutic potential of targeting CD36 in stroke.

Main Methods:

  • Literature review of studies on CD36 pathways and stroke.
  • Analysis of CD36's role in inflammation and endothelial dysfunction.

Main Results:

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Last Updated: May 22, 2026

Embryonic Stem Cell-Derived Endothelial Cells for Treatment of Hindlimb Ischemia
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Embryonic Stem Cell-Derived Endothelial Cells for Treatment of Hindlimb Ischemia

Published on: January 23, 2009

Endothelin-1 Induced Middle Cerebral Artery Occlusion Model for Ischemic Stroke with Laser Doppler Flowmetry Guidance in Rat
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Endothelin-1 Induced Middle Cerebral Artery Occlusion Model for Ischemic Stroke with Laser Doppler Flowmetry Guidance in Rat

Published on: February 16, 2013

  • CD36 activation by various ligands triggers inflammatory responses.
  • These responses contribute to endothelial dysfunction, a factor in cardiovascular and cerebrovascular diseases.
  • CD36 signaling pathways are implicated in stroke pathology.

Conclusions:

  • Targeting CD36 presents a promising therapeutic avenue for stroke.
  • Understanding CD36-ligand interactions is crucial for developing effective stroke treatments.