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Updated: Jun 27, 2026

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08:22

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Published on: April 15, 2020

Extracellular Vesicles Link Cerebral Ischemia to Coronary Microvascular Dysfunction - Role for RGD Motif-Activated

Marta Balogh1, Melina Tangos2,3,4, Vijay S Patel5

  • 1Department of Physiology, Medical College of Georgia, Augusta University, Augusta, GA, 30912, USA.

Journal of Cardiovascular Translational Research
|June 25, 2026
PubMed

Insights

Ischemic stroke impairs heart blood vessel function through circulating factors. This study reveals extracellular vesicles mediate this brain-heart connection, offering potential therapeutic targets.

Area of Science:

  • Cardiovascular Research
  • Neurology
  • Vascular Biology

Background:

  • Ischemic stroke increases the risk of subsequent cardiac ischemic events.
  • Mechanisms linking cerebral ischemia to coronary dysfunction are not fully understood.
  • Circulating factors released after cerebral ischemia may directly impair coronary microvascular function.

Purpose of the Study:

  • To investigate whether ischemic stroke directly impairs coronary microvascular function.
  • To identify the role of circulating factors, specifically extracellular vesicles, in this process.
  • To elucidate the signaling pathways involved in stroke-induced coronary dysfunction.

Main Methods:

  • Assessed coronary arteriole (CA) vasodilator function in patients with prior ischemic stroke.
  • Utilized a rat model of transient middle cerebral artery occlusion (MCAO).
  • Isolated extracellular vesicles (EVs) from post-ischemic rats and delivered them into rat CA lumen.
  • Administered RGD peptide and endothelin ETA receptor antagonist (BQ-123) to rat CAs.

Main Results:

  • Coronary arteriole vasodilator function was reduced in patients with prior ischemic stroke.
  • MCAO in rats impaired CA vasodilator function.
  • EVs from ischemic rats impaired vasodilation when delivered into rat CAs.
  • RGD peptide attenuated flow-induced vasodilation, an effect blocked by BQ-123.

Conclusions:

  • Ischemic stroke directly induces coronary microvascular dysfunction.
  • Circulating extracellular vesicles play a key role in the brain-heart vascular axis.
  • RGD-motif-dependent activation of endothelin signaling mediates stroke-induced coronary dysfunction.
  • EV-mediated pathways represent potential therapeutic targets for post-stroke cardiac risk.

Keywords:
Arginine-Glycine-Aspartic AcidEndothelinEndotheliumIschemic StrokeMicroparticleMyocardial IschemiaVesicle

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