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Review
. 2022 Dec 1;13(6):1770-1786.
doi: 10.14336/AD.2022.0416.

Exosomes as a Cell-free Therapy for Myocardial Injury Following Acute Myocardial Infarction or Ischemic Reperfusion

Ziyu An #  1 , Jinfan Tian #  1 , Yue Liu  2 , Xin Zhao  1 , Xueyao Yang  1 , Jingwen Yong  1 , Libo Liu  1 , Lijun Zhang  1 , Wenjian Jiang  3 , Xiantao Song  1 , Hongjia Zhang  3
Affiliations
Review

Exosomes as a Cell-free Therapy for Myocardial Injury Following Acute Myocardial Infarction or Ischemic Reperfusion

Ziyu An et al. Aging Dis. .

Abstract

Exosomes, which contain miRNA, have been receiving growing attention in cardiovascular therapy because of their role in mediating cell-cell communication, autophagy, apoptosis, inflammation, and angiogenesis. Several studies have suggested that miRNA derived from exosomes can be used to detect myocardial infarctions (MI) in patients. Basic research also suggests that exosomes could serve as a potential therapeutic target for treating acute myocardial infarction. Ischemia/reperfusion (IR) injury is associated with adverse cardiac events after acute MI. We aim to review the potential benefits and mechanisms of exosomes in treating MI and IR injury.

Keywords: acute myocardial infarction; cell-free therapy; exosome; ischemic reperfusion.

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Conflict of interest statement

Competing interests The authors declare no competing interests

Figures

Figure 1.
Figure 1.
Partial anti-inflammatory properties of exosomes after MI or IR. Note: Exosomes produced by M2 macrophages (M2-exo) carrying miR-148a down-regulate thioredoxin-interaction protein (TXNIP) to reduce MI or I/R damage. In addition, M2-exo can carry miR-1271-5P to negatively regulate SOX6 expression and inhibit myocardial apoptosis. Mesenchymal stem cells derived exosomes (MSCs-exo) promote M2 polarization of macrophages and improve myocardial injury after myocardial infarction by activating the S1P/SK1/S1PR1 signaling pathway. Exosomes from Ang II-treated atrial myocytes promote the polarization of M2 macrophages by delivering miR-23a. In contrast, M1-Exo overexpressed inflammatory miR-155, aggravating the myocardial injury.
Figure 2.
Figure 2.
Partial anti-apoptosis properties of exosomes after MI or IR. Note: Bone marrow mesenchymal stem cells derived exosomes (BMMSCs-exo) increased miR-150-5p expression and decreased Bax expression in MI mice. The level of miR-24 was up-regulated, and the protein expressions of Bax and Caspase-3 were down-regulated. Overexpression of miR-338 by BMMSCS-exo decreased the expression of Bax, increased the expression of Bcl-2, and significantly reduced apoptosis. The expression of miR-25-3p in bone marrow mesenchymal stem cells derived exosomes (BMMSCS-exo) targets the pro-apoptotic gene PTEN and reduces its protein level. MiR-486-5p in bone marrow stromal cell-derived exosomes inhibits PTEN expression. In addition, miR-221 secreted by GATA4-exo down-regulated PTEN expression and reduced apoptosis. BMMSCs-exo expression of miR-185 reduces SOCS2 expression to protect against myocardial apoptosis.
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