Table 1.
Different miRNAs and their influence on pathophysiological pathways involved in myocardial infarction or after infarction.
| miRNAs | Cardiac Processes | Biological Pathways | Ref. |
|---|---|---|---|
| miR-378 | Modulates cardiac fibrosis | PCFL regulates cardiac fibrosis via miR-378/GRB2 pathway; | [47] |
| miR-101 | Cardiac fibrosis | By decreasing c-Fos and its downstream TGF-β1 | [48] |
| miR-208a | Apoptosis | By Upregulating Bax; | [49] |
| miR-208a | Promoted apoptosis and oxidative stress | By regulation of protein tyrosine phosphatase receptor type G and protein tyrosine phosphatase; non-receptor type 4 | [50] |
| miR-208a | Myocardial fibrosis | via upregulation of endoglin; | [51] |
| miR-208a | Cardiac hypertrophy and fibrosis | Via upregulation of endoglin after activation by TGF-β1; | [52] |
| miR-223 | Cardiac fibrosis | By negatively regulating RASA1 expression, and it mediates the pro-fibrotic effects of TGF-β1 in vitro; | [53] |
| miR-133a | Apoptosis suppressor | By inhibiting TAGLN2, HSP60, HSP70, Apaf-1, caspase-3/8/9 expression, and promoting antiapoptotic protein Bcl-2 expression, and by regulating caspase-9. | [54] |
| miR-133a | Inhibits angiogenesis, | By targeting SRF; | [55] |
| miR-133a | Inhibits angiogenesis, | Via VEGFR2 and fibroblast growth factor receptor 1; | [56] |
| Anti-apoptotic role | By inhibiting proapoptotic genes: death-associated protein kinase 2 (DAPK2), apoptotic protease activating factor 1 (APAF1), caspase-9, Bcl-2-like 11, and Bcl-2-modifying factor (BMF); | [57] | |
| MiRNA-23a | Cardiac apoptosis | By suppressing the expression of manganese superoxide dismutase. | [58] |
| miR-26a-5p | Cardiac fibrosis | Regulation of cardiac collagen I expression by targeting ULK1; | [59] |
| miRNA-26b | Relieves inflammatory response | By suppression of mitogen-activated protein kinase (MAPK) pathway through binding to Prostaglandin-Endoperoxide Synthase 2 (PTGS2); | [60] |
| miRNA-144 | Oxidative stress | Through regulation of Forkhead Box O1; | [61] |
| miRNA-24-3p | Reduces apoptosis | Via regulation of Keap1-Nrf2 pathway in response to ischemia/reperfusion injury; | [62] |
| miR-21 | Attenuates inflammation | Through targeting kelch repeat and BTB (POZ) domain containing 7 and inhibiting p38 and NF-κB signaling activation; | [63] |
| miRNA-143-3p | Promotes fibrosis | By activation of P38, ERK, and JNK pathways; | [64] |
| miRNA27a, miRNA-28-3p, miRNA-34a |
Contribute to oxidativestress | By the inhibition of Nrf2 translation in chronic heart failure post-MI; contributing to the dysregulation of the Nrf2/ARE signaling pathway; | [65] |
| miRNA-320 | Cardiomyocyte death and apoptosis | By regulating small heat-shock protein 20 (Hsp20) protein synthesis; | [65] |
| miR-200a | Reduce inflammation | By targeting the Keap1/Nrf2 and β-catenin pathways; | [66] |
| miR-6391, miR-671, miR-558, miR-1538 |
Apoptosis in the non-infarcted areas after MI |
Regulation of the proteins involved in the synthesis and signaling cascade of sphingolipids; | [65] |
| miR-6391 | Tissue remodeling | Via regulation of the neurotrophin signaling pathway; | [67] |
| miR-25, miR-3535, miR-6391 | Cardiac fibrosis | Via downregulation of collagen organization. | [68] |
microRNA (miRNA); pro-cardiac fibrotic lncRNA (PCFL); growth factor receptor bound protein 2 (GRB2); myocardial infarction (MI); transforming growth factor-β1 (TGF-β1); bcl-2-associated X-protein (Bax); RAS p21 protein activator (GTPase-activating protein) (RASA1); serum response factor (SRF); vascular endothelial growth factor receptor 2 (VEGFR2); unc-51-like autophagy activating kinase 1; antioxidant response element (ARE); nuclear factor-erythroid factor 2-related factor 2 (Nrf2); Kelch-like ECH-associated protein 1 (Keap1).