The Application Potential and Advance of Mesenchymal Stem Cell-Derived Exosomes in Myocardial Infarction
Table 1
List of components of the MSC-derived exosome molecular cargo to regulate cardiac repairment published in the recent 5 years.
Diseases
Component
Type of MSCs
Target cell
Function
Reference
Cardiac preservation
Mouse MI
miR-214
ADRC
CM
ADRC-derived exosomes inhibited cardiomyocyte cell damage under hypoxia in vitro, decreased infarcted size, and improved cardiac function through miR-214-regulated clathrin endocytosis.
Exosomes from hypoxia-conditioned BMSCs can facilitate cardiac repair and ameliorate CM apoptosis through suppressing the expression of the proapoptotic genes p53 and BAK1.
MSC-derived exosomes protect NMCM from hypoxia and serum deprivation-induced autophagic flux, decreased infarct size, and improved cardiac function via miR-125b-mediated p53-Bnip3 signaling.
Exosomes from ischemic preconditioned BMSCs resulted in antiapoptotic effect on CMs due to ischemia by targeting Mecp2 and displayed reduced cardiac fibrosis.
BMSC-derived exosomes protected CMs against oxygen-glucose deprivation-induced apoptosis by directly targeting the proapoptotic genes (FASL and PTEN) and EZH2 to confer cardioprotective effects and suppress inflammation post-I/R injury.
miR-146a containing exosomes had more effect than the normal exosome treatment group on the suppression of AMI-induced apoptosis, inflammatory response, and fibrosis in an AMI rat model through interacting with the 3-untranslated region of EGR1.
miR-210-overexpressing MSC exosomes exerted myocyte protection by targeting AIFM3 to inhibit NRCM apoptosis and reduce infarct size and improve heart function in the rat MI model.
GATA-4-overexpressing MSC-derived exosomes contributed to increased CM survival, reduced CM apoptosis, and preserved mitochondrial membrane potential in CM under a hypoxic environment by targeting PTEN to activate the Akt and ERK signaling.
Exosomes secreted from BMSCs transfected with miR-338 mimic decreased the apoptosis of H9C2 and improved cardiac function by regulating the MAP3K2/JNK signaling pathway.
miR-133-overexpressing BMSC-derived exosomes inhibited hypoxia-induced NRCM apoptosis and repressed inflammatory level and the infarct size by targeting snail 1.
BMSC-derived exosomes enriched with miR-29 and miR-24 enhanced cardiac repair by promoting CM proliferation, reducing apoptosis induced by H2O2, and inhibiting fibrosis of fibroblast cell induced by TGF-β.
EnMSCs showed superior cardioprotective effects through antiapoptotic and angiogenic effects by enhancing cell survival through the miR-21/PTEN/Akt pathway.
miR-486-5p carried by BMSC-derived exosomes promoted the H9C2 proliferation and rescued H9C2 cells from hypoxia/reoxygenation-induced apoptosis by suppressing PTEN expression and activating the PI3K/AKT signaling pathway.
Exosomes obtained from MIF-pretreated hAD-MSCs exhibited a protective effect on CM cells from hiPSC differentiation through the lncRNA-NEAT1/miR-142-3p/FOXO1 pathway.
miR-210 in BMSC-secreted exosomes improved angiogenesis by increasing the proliferation, migration, and tube formation capacity of HUVECs and contributed to cardiac protection.
The exosomes from SIRT1-overexpressing ADSCs can restore the function of cell migration and tube formation and recruitment of EPCs to the repair area through Nrf2/CXCL12/CXCR7 signaling.
Exosomes from atorvastatin preconditioned MSCs can regulate the expression of miR-675 and activation of VEGF and intercellular adhesion molecule-1 to promote angiogenesis.
Overexpression of miRNA-181a in hUCB-MSC-derived exosomes suppressed inflammatory response in the PBMCs and promoted Treg cell polarization through targeting c-Fos.
Exosomes obtained from LPS preconditioning BMSCs strongly increased M2 macrophage polarization and attenuated the postinfarction inflammation in the MI model through inhibition of LPS-dependent NF-κB signaling pathway and activation of the AKT1/AKT2 signaling pathway.
hUC-MSC-derived exosomes suppressed myofibroblast formation by inhibiting excess α-smooth muscle actin and collagen deposition via the activity of the TGF-β/SMAD2 signaling pathway.
