TABLE 1.
Regulatory role of miRNAs from cardiac cells-derived exosomes in various cell crosstalk.
| Donor cells | Recipient cells | Enriched miRNA | Regulatory role | References |
|---|---|---|---|---|
| CMs after MI | Normal CMs | miR-328-3p | miR-328-3p regulates the Caspase signaling pathway and promotes the apoptosis of normal CMs. | Huang et al. (2021) |
| CMs treated with epigallocatechin gallate | I/R-induced CMs | miR-30a | miR-30a inhibits CMs apoptosis and autophagy induced by I/R by increasing the average diameter and concentration of CMs exosomes as well as the expression level of miR-30a mRNA and specific protein in exosomes. | Zhang et al. (2020) |
| Fibrotic CMs | Normal FBs | miR-208a | miR-208a inhibits the expression of DYRK2 in FBs, promotes the dephosphorylation of activated T nuclear factor in the cytoplasm, and then promotes the proliferation of FBs and the transformation into myoblasts. | Yang et al. (2018) |
| Hypoxic CMs | FBs | miR-208a/b | miR-208a/b inhibits the apoptosis of FBs, promotes survival and migration, enhances the accumulation of α-SMA, type I collagen, type III collagen, reactive oxygen species, malonaldehyde, and Fe2+, and inhibits the expression of GPX4, a key regulator of iron death. | Guo et al. (2023) |
| Hypertrophic CMs stimulated by mechanical overstretch for 24 h | FBs | miR-494-3p | miR-494-3p regulates FBs activation by inhibiting PTEN expression and activating the AKT/Smad2/3/ERK signaling pathway and is closely related to the occurrence and development of myocardial fibrosis caused by stress overloading. | Tang (2020) |
| H9c2 transfected with miR-217 mimics | FBs | miR-217 | miR-217 targets PTEN to enhance the proliferation of FBs and participate in cardiac hypertrophy and fibrosis. | Nie et al. (2018) |
| CMs after MI | FBs after MI | miR-195 | miR-195 is significantly upregulated in CMs-derived exosomes and can be transferred to FBs to participate in MFBs activation. | Morelli et al. (2019) |
| CMs treated with H2O2 for 3 h | ECs treated with H2O2 for 3 h | miR-19a-3p | miR-19a-3p inhibits ECs proliferation and tubular formation by down-regulating HIF-1α protein levels, and induces, cell death. | Gou et al. (2020) |
| CMs from Goto-Kakizaki rats | ECs | miR-320 | miR-320 inhibits ECs proliferation, migration, and tubular formation. | Wang et al. (2014) |
| CMs stimulated by phenylephrine and isoproterenol | ECs | miR-200c-3p | miR-200c-3p inhibits ECs proliferation, migration and tubule formation. | Ottaviani et al. (2019) |
| Hypoxic CMs | Gli1+ cells | miR-223 | miR-223 significantly up-regulates the levels of Gli1+ fibrosis-associated protein α-SMA, collagen receptor-discoid domain receptor 2, and type I collagen. | Lin et al. (2019) |
| Angiotensin II-induced CMs | Macrophages | miR-155 | miR-155 induces ERK, JNK, and p38 through the enrichment of miR-155, thereby stimulating the inflammatory response of macrophages. | Yu et al. (2021) |
| Atrial muscle cells treated with angiotensin II | Macrophages | miR-130 | miR-130 promotes M1-type polarization of macrophages. | Huang et al. (2022) |
| Oxidative stress-induced CMs | Macrophages | miR-106b-5p | miR-106b-5p promotes M1-type polarization of macrophages. | Li et al. (2023) |
| CMs induced by oxidative stress | Hypoxic H9c2 | miR-423-3p | miR-423-3p promotes M1-type polarization of macrophages. | Luo et al. (2019) |
| cCFU-FBs overexpressed by GATA4 gene | H9c2 | miR-221 | miR-221 inhibits the expression of PTEN and activates the PTEN/PI3K/AKT signaling pathway, thereby alleviating the apoptosis of CMs. | Hao et al. (2020) |
| I/R injury-induced FBs | CMs | miR-133a | miR-133a targets ELAVL1 to inhibit the pyrodeath of CMs, thereby protecting CMs. | Liu et al. (2022) |
| Fibroblasts subjected to mechanical stretch for 48 h | CMs | miR-143 | miR-143 promotes apoptosis of CMs. | Zhang (2018) |
| FBs | CMs | miR-21-3p | miR-21-3p inhibits CMs targets SORBS2 and PDLIM5 and induce CMs hypertrophy. | Bang et al. (2014) |
| FBs treated with TGF-β1 | CMs | miR-200a-3p | miR-200a-3p inhibits the expression of VEGFA, HIF-1α, CD31, and angiopoietin 1 gene, inhibits proliferation, migration, and tubular formation, and promotes apoptosis. | Ranjan et al. (2021) |
| Atrial MFBs induced by angiotensin II | CMs | miR-21-3p | miR-21-3p down-regulates the expression of L-type calcium channel Cav1.2, a marker of ionic remodeling associated with atrial fibrillation in CMs, which may be a key substance in increasing the susceptibility to atrial fibrillation in the process of atrial fibrosis. | Li et al. (2020) |
| Sca-1+ CPCs after MI | CPCs induced by H2O2 | miR-133a | miR-133a promotes CPCs survival under oxidative stress by decreasing Caspase-3 activity and targeting the expression of pro-apoptotic genes Bim and Bmf. | Izarra et al. (2014) |
| CPCs induced by oxidative stress | H9c2 | miR-21 | miR-21 down-regulates PDCD4 and inhibits oxidative stress-induced apoptosis of H9c2 cells. | Xiao et al. (2016) |
| CPCs | CMs and ECs | miR-210 and miR-132 | miR-210 inhibited CMs apoptosis by down-regulating its target ephrin A3 and PTP1b; miR-132 enhanced tubular formation in ECs by down-regulating its target RasGAP-p120. | Barile et al. (2014) |
| Sca-1+ CPCs | HL-1 cells | pre-miR-323-5p, pre-miR-181a, and pre-miR-132 | Enhance cell tolerance to H/R damage. | Cervio et al. (2014) |
| Endogenous GATA4 positive CPCs | H9c2 | miR-222 | miR-222 protects H9c2 cells from apoptosis by mediating the PTEN-PI3K/AKT signalling pathway and improves their survival rate. | Yu et al. (2015) |
| CPCs | H9c2 treated with H2O2 for 4 h | miR-451 | miR-451 protects H9c2 cells from oxidative stress by inhibiting the activation of Caspase-3/Caspase-7. | Chen et al. (2013) |
| CPCs | iPSCs-derived CMs or CMs from newborn rats | miR-528-3p and miR-7641 | miR-528-3p and miR-7641 induced the proliferation of stationary CMs. | Sharma et al. (2018) |
| CPCs treated with doxorubicin | CMs induced by doxorubicin or trastuzumab | miR-146a-5p | miR-146a-5p attenuates oxidative stress damage induced by adriamycin/trastuzumab by inhibiting the expression of Traf6 and Mpo. | Milano et al. (2020) |
| CPCs | CMs and ECs | miR-210, miR-146a and miR-132 | miR-210 and miR-146a inhibited apoptosis of CMs by down-regulating ephrinA3/PTP1b signaling pathway and Nox4 target protein. miR-132 plays a pro-angiogenic role by down-regulating the target protein RasGAP-p120. | Barile et al. (2015) |
| Bioengineered CPCs transfected by pro-angiogenic miR-322 | ECs | miR-322 | miR-322 promotes angiogenesis. | Youn et al. (2019) |
| Hypoxic induced CMECs | H/R-induced H9c2 | miR-27b-3p | miR-27b-3p down-regulates the expression of GSDMD, NLRP3 and Caspase-1 in H9c2 cells by regulating Foxo1/GSDMD axis, thereby inhibiting pyroptosis. At the same time, the serum creatine kinase isozyme, lactate dehydrogenase, interleukin-1β, and interleukin-18 levels were significantly reduced. | Zhang (2023) |
| CDCs | H2O2-induced CMs | miR-146a, miR-22, miR-24, miR-210, etc. | miR-146a, miR-22, miR-24, miR-210, etc. inhibited CMs apoptosis and promoted cell proliferation. | Ibrahim et al. (2013) |
| Hypoxic CDCs | HUVECs | miR-126, miR-130a, miR-210, and other pro-angiogenic miRNAs | miR-126, miR-130a, miR-210, and other pro-angiogenic miRNAs promote tubular formation of HUVECs. | Namazi et al. (2018) |
| CDCs | Macrophages after ischemic preconditioning | miR-181b | miR-181b is an important candidate mediator for CDCs-induced macrophage polarization and plays a cardioprotective role by reducing PKCδ transcription levels. | de Couto et al. (2017) |
| CMs after MI | Tumor cells | miR-22-3p | miR-22-3p directly targets the ACSL4 gene of tumor cells, thereby inhibiting cell iron death induced by the eradicator of Ras and ST and accelerating tumor progression. | Yuan et al. (2023) |
| CMs after MI | Bone marrow progenitor cells | miR-1, miR-208, and miR-499 | miR-1, miR-208, and miR-499 inhibited CXCR4 expression and increased the number of CPCs. | Cheng et al. (2019) |
α-SMA, α smooth muscle actin; ACSL4, acyl-CoA synthetase long chain family member 4; AMI, acute myocardial infarction; cCFU-FBs, cardiac colony-forming unit fibroblasts; CMECs, cardiac microvascular endothelial cells; CMs, cardiomyocytes; CPCs, cardiac progenitor cells; CXCR4, C-X-C motif chemokine receptor 4; DYRK2, dual specificity tyrosine phosphorylation regulated kinase 2; ECs, endothelial cells; ELAVL1, ELAV-like RNA binding protein 1; ERK, extracellular regulated kinase; FBs, fibroblasts; GPX4: glutathione peroxidase 4; H/R, hypoxia/reoxygenation; HIF-1α, hypoxic inducible factor-1 α; UVECs, human umbilical vein endothelial cells; I/R; ischemia-reperfusion; iPSCs, induced pluripotent stem cells; JNK, c-Jun N-terminal kinase; MFBs, myofibroblasts; MI, myocardial infarction; miRNA, microRNA; PDCD4: programmed cell death 4; PTEN, tensin homolog deleted on chromosome ten; TGF-β1, transforming growth factor-β1; VEGFA, vascular endothelial growth factor A.