Table 2.

Preclinical studies evaluating the effect of exosomal miRNAs in myocardial infarction

miRNA	Expression	Donor cell	Recipient cell	Exosome isolation	Main function
miR-21112	upregulation	patient serum	cardiomyocytes	kit	reduce the infarct size and cell apoptosis through PDCD4 downregulation
miR-21113	upregulation	HEK293T	cardiomyocytes and HUVECs	ultracentrifugation	reduce PDCD4 expression and attenuate cell apoptosis
miR-21-5p111	upregulation	CTs	HMVECs	ultracentrifugation	suppress apoptosis and promote the survival of HMVECs and angiogenesis
miR-24114	upregulation	BMSCs	cardiomyocytes and H9c2	ultracentrifugation	inhibit cardiomyocyte apoptosis and improve myocardial function
miR-25-3p115	upregulation	BMSCs	cardiomyocytes	ultracentrifugation	reduce apoptosis and cytokine expression
miR-30e116	upregulation	BMSCs	cardiomyocytes	ultracentrifugation	inhibit LOX1 expression, downregulate the activity of the NF-κB p65/caspase-9 signaling, and ameliorate heart failure
miR-31117	upregulation	ADSCs	HMVECs	ultracentrifugation	promote HMVEC migration and tube formation by targeting FIH1
miR-98-5p142	upregulation	BMSCs	cardiomyocytes	ultracentrifugation	suppress myocardial enzyme levels, oxidative stress, inflammation response, macrophage infiltration, and infarct size
miR-125b118	upregulation	BMSCs	cardiomyocytes	ultracentrifugation	ameliorate cardiomyocyte apoptosis and cardiac damage
miR-126119	upregulation	ADSCs	cardiomyocytes and EPCs	ultracentrifugation	protect myocardial cells from apoptosis, inflammation, and fibrosis and boost angiogenesis
miR-126120	downregulation	ECs	cardiomyocytes	ultracentrifugation	severe cardiac dysfunction and hypertrophy
miR-129121	upregulation	HUVECs	cardiomyocytes	ultracentrifugation	downregulate TLR4 and disrupt the NF-κB signaling and NLRP3 inflammasome to protect against I/R injury
miR-129-5p122	upregulation	BMSCs	cardiomyocytes	ultracentrifugation	decrease inflammatory cytokine expression, apoptosis, and fibrosis
miR-132123	downregulation	CPCs	ECs	ultracentrifugation	enhance tube formation via downregulating RasGAP-p120
miR-133a-3p124	upregulation	ucMSCs	cardiomyocytes, H9c2, and HUVECs	ultracentrifugation	promote angiogenesis, inhibit apoptosis, reduce fibrosis, and preserve heart function
miR-143125	upregulation	SMCs	ECs	ultracentrifugation	regulate angiogenesis by reducing the proliferation index of ECs and their capacity to form vessel-like structures
miR-143110	downregulation	patient serum	HUVECs	ultracentrifugation	promote cell proliferation, migration, and tube formation
miR-145125	upregulation	SMCs	ECs	ultracentrifugation	regulate angiogenesis by reducing the proliferation index of ECs and the capacity to form vessel-like structures
miR-146a126	upregulation	ADSCs	cardiomyocytes and H9c2	ultracentrifugation	suppress apoptosis and inflammatory response
miR-150-5p127	upregulation	BMSCs	cardiomyocytes	ultracentrifugation	decrease Bax expression, alleviate pathological changes of the myocardium, decrease apoptosis rate, and improve cardiac function
miR-153-3p128	downregulation	BMSCs	H9c2 and ECs	ultracentrifugation	reduce the apoptosis by promoting ANGPT1 expression and VEGF/VEGFR2/PI3K/Akt/eNOS pathway activation
miR-185129	upregulation	BMSCs	cardiomyocytes	ultracentrifugation	repress ventricular remolding by inhibiting SOCS2
miR-208b143	upregulation	patient plasma	HUVECs	ultracentrifugation	suppress cell viability and migration and promote cell apoptosis by regulating Bcl2 and Bax and the FAK/MAPK1/Raf-1 pathway
miR-210123	downregulation	CPCs	cardiomyocytes	ultracentrifugation	inhibit apoptosis by downregulating ephrin A3 and PTP1b
miR-210130	upregulation	BMSCs	cardiomyocytes	ultracentrifugation	increase cardiomyocytes viability, improve heart function, and reduce cardiac fibrosis
miR-210131	downregulation	BMSCs	HUVECs	ultracentrifugation	improve angiogenesis and cardiac function
miR-212-5p132	upregulation	BMSCs	cardiomyocytes	ultracentrifugation	protect against cardiac fibrosis
miR-218-5p133	upregulation	EPCs	cardiomyocytes	ultracentrifugation	promote CF proliferation and inhibit myocardial fibrosis
miR-223134	upregulation	ucMSCs	HUVECs and H9c2	ultracentrifugation	facilitate angiogenesis of HUVECs, repress inflammatory response and apoptosis, and promote angiogenesis in cardiomyocytes
miR-322135	upregulation	CPCs	HUVECs	ultracentrifugation	promote angiogenesis via the upregulation of Nox2
miR-328-3p136	upregulation	cardiomyocytes	cardiomyocytes	ultracentrifugation	promote the activation of the caspase pathway and apoptosis
miR-338137	upregulation	MSCs	cardiomyocytes and H9c2	ultracentrifugation	inhibit H2O2-induced apoptosis and improve cardiac function by regulating MAP3K2/JNK signaling pathway
miR-363-3p133	upregulation	EPCs	cardiomyocytes	ultracentrifugation	promote CF angiogenesis and inhibit myocardial fibrosis
miR-486-5p138	upregulation	BMSCs	CFs and ECs	ultracentrifugation	promote angiogenesis by downregulating fibroblast MMP19 and increase the potency of myocardial repair
miR-494-3p140	upregulation	BMDCs	CMECs	ultracentrifugation	enhance tube formation and promote angiogenesis
miR-671140	upregulation	adMSCs	cardiomyocytes	ultracentrifugation	alleviate fibrosis and cell apoptosis
miR-4732-3p141	upregulation	MSCs	cardiomyocytes and HUVECs	ultracentrifugation	induce angiogenesis and inhibit myofibroblast differentiation and the production of extracellular matrix

BMSCs, bone marrow-derived mesenchymal stem cells; LOX1, lectin-like oxidized low-density lipoprotein receptor-1; SOCS2, suppressor of cytokine signaling 2; adMSCs, adipose-derived mesenchymal stem cells; HUVECs, human umbilical vein endothelial cells; TLR4, Toll-like receptor 4; NLRP3, NOD-like receptor 3; I/R, ischemia-reperfusion; ADSCs, adipose-derived stem cells; EPCs, endothelial progenitor cells; ucMSCs, umbilical cord mesenchymal stem cells; EGR1, early growth response factor 1; CFs, cardiac fibroblasts; ECs, endothelial cells; HIF1, hypoxia-inducible factor-1; HMVECs, human microvascular endothelial cells; CPCs, cardiac progenitor cells; NOX, NADPH oxidase; MMP19, matrix metalloproteinase 19; BMDCs, bone marrow-derived dendritic cells; CMECs, cardiac microvascular endothelial cells; SMCs, smooth muscle cells; CTs, cardiac telocytes.