Treatment of oxidative stress with exosomes in myocardial ischemia

Yun Liu, Mengxue Wang, Yin Liang, Chen Wang, Keiji Naruse, Ken Takahashi

Research output: Contribution to journalReview articlepeer-review

18 Citations (Scopus)


A thrombus in a coronary artery causes ischemia, which eventually leads to myocar-dial infarction (MI) if not removed. However, removal generates reactive oxygen species (ROS), which causes ischemia–reperfusion (I/R) injury that damages the tissue and exacerbates the resulting MI. The mechanism of I/R injury is currently extensively understood. However, supplementation of exogenous antioxidants is ineffective against oxidative stress (OS). Enhancing the ability of endogenous antioxidants may be a more effective way to treat OS, and exosomes may play a role as targeted carriers. Exosomes are nanosized vesicles wrapped in biofilms which contain various complex RNAs and proteins. They are important intermediate carriers of intercellular communication and material exchange. In recent years, diagnosis and treatment with exosomes in cardiovascular diseases have gained considerable attention. Herein, we review the new findings of exosomes in the regulation of OS in coronary heart disease, discuss the possibility of exosomes as carriers for the targeted regulation of endogenous ROS generation, and compare the advantages of exosome therapy with those of stem-cell therapy. Finally, we explore several miRNAs found in exosomes against OS.

Original languageEnglish
Article number1729
Pages (from-to)1-18
Number of pages18
JournalInternational journal of molecular sciences
Issue number4
Publication statusPublished - Feb 2 2021


  • Coronary heart disease
  • Exosome
  • Exosome therapy
  • Myocardial infarction
  • Oxidative stress
  • Reactive oxygen radicals

ASJC Scopus subject areas

  • Catalysis
  • Molecular Biology
  • Spectroscopy
  • Computer Science Applications
  • Physical and Theoretical Chemistry
  • Organic Chemistry
  • Inorganic Chemistry


Dive into the research topics of 'Treatment of oxidative stress with exosomes in myocardial ischemia'. Together they form a unique fingerprint.

Cite this