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Table 3 Sources, cargo, pathways and biological effects of exosomes secreted by cardiac cells under the indicated conditions

From: Advances in the study of exosomes derived from mesenchymal stem cells and cardiac cells for the treatment of myocardial infarction

Source of exosomes

Condition

Cargos

Pathways

Biological effects

Reference

Cardiomyocytes

MI

miR-328-3p↑

miR-328-3p/Caspase

apoptosis↑

[108]

Cardiomyocytes

MI

miR-19a-3p↑

miR-19a-3p/HIF-1α

angiogenesis↓

[109]

Cardiomyocytes

Hypoxia

lncRNA AK139128↑

not investigated

apoptosis↑

[110]

Cardiomyocytes

Ferroptosis

miR-106b-3p↓

miR-106b-3p/Wnt/macrophage polarization to M1

inflammation↑

[80]

Cardiomyocytes

Hypoxia

not investigated

macrophage polarization to M2

inflammation↓

[111]

Cardiomyocytes

Hypoxia

miR-208a

miR-208a/Dyrk2

fibrosis↑

[112]

Cardiomyocytes

Ischemia

miR-222; miR-143

not investigated

angiogenesis↑

[113]

Cardiomyocytes

Hypoxia

circHIPK3

circHIPK3/miR-29a/VEGFA

angiogenesis↑

[114]

Cardiomyocytes

Ischemia

lncRNA KLF3-AS1↑

lncRNA KLF3-AS1/miR-23c/STAT5B

apoptosis↓

[115]

CDCs

Normal/Hypoxia

Not investigated

not investigated

apoptosis↓

[116]

CDCs

Normal/Hypoxia

miR-126; miR-130a; miR-210

not investigated

angiogenesis↑

[117]

CDCs (EVs)

I/R

Y RNA fragment

Y RNA fragment/IL10

cardioprotection↑, infarct size↓

[118]

CDCs

Normal

miR-181b

miR-181b/PKCδ/macrophages polarization

cardioprotection↑, infarct size↓

[119]

ECs

MI

PFN2

PFN2/PI3K-PFN2-ERK

angiogenesis↑

[120]

ECs

Normal

not investigated

PI3K-AKT

apoptosis↓

[121]

ECs

Normal

LINC00174

LINC00174/SRSF1/P53/AKT-AMPK

apoptosis↓, autophagy↓

[122]

ECs (EVs)

MI

VCAM-1

VCAM-1/neutrophil mobilization

not investigated

[123]

Endothelial progenitor cells

Normal

miR-1246; miR-1290

miR-1246/ELF5, miR-1290/SP1

angiogenesis↑

[124]

Endothelial progenitor cells

Normal

miR-218-5p; miR-363–3

miR-218-5p/p53, miR-363–3/JMY

angiogenesis↑

[125]

Cardiac-resident progenitor cells

Patients undergoing heart surgery for aortic valve disease and/or coronary artery disease

PAPP-A

PAPP-A/IGF-1

apoptosis↓

[126]

Cardiac progenitor cells

Patients undergoing open-chest surgery

not investigated

MAPK/ERK1/2

inflammation↓, angiogenesis↑

[127]

Cardiac telocytes

Normal

miR-21-5p

miR-21-5p/Cdip1/caspase-3

apoptosis↓, angiogenesis↑

[128]

CFs

Hypoxia/reoxygenation

miR-133a↑

miR-133a/ELAVL1

pyroptosis↓

[129]

Epicardial cells

I/R

miR-30a; miR-100; miR-27a; miR-30e

not investigated

cardiomyocyte proliferation↑

[130]

  1. AKT protein kinase B, AMPK adenosine 5 ‘-monophosphate (AMP)-activated protein kinase, CDCs cardiosphere-derived cells, Cdip1 cell death inducing protein 1, CFs cardiac fibroblasts, Dyrk2 dual specificity tyrosine (Y) phosphorylation regulated kinase 2, ECs endothelial cells, ELAVL1 ELAV-like RNA-binding protein 1, ELF5 E74-like factor 5, ERK1/2 Extracellular regulated protein kinase 1/2, EVs extracellular vesicles, HIF-1α hypoxia-inducible factor 1, I/R ischemia/reperfusion, IGF-1 insulin-like growth factor 1, IL10 interleukin 10, JMY regulatory protein, MAPK mitogen-activated protein kinase, MI myocardial infarction, PAPP-A pregnancy-associated plasma protein-A, PI3K phosphatidylinositol3-kinase, PKCδ protein kinase C δ, SP1 specificity protein 1, SRSF1 serine and arginine rich splicing factor 1, STAT5B signal transducer and activator of transcription 5B, PFN2 profilin 2, VCAM-1 vascular cell adhesion molecule 1, VEGFA vascular endothlial growth factor A