Table 1.
Summary of miRNAs involved in the diseases’ pathogenesis
| miRNA | Disease | Type of Model of Study | Description of model of study | Exerted Effect | Mechanism of Action | Reference |
|---|---|---|---|---|---|---|
| miR-19b-3p | AKI and CKD | In vivo | LPS-induced AKI mice | Amplification of inflammatory response by promotion of M1 macrophage polarization and activation of NF-κB signaling | Activation of NF-κB signaling targeting SOCS1 | Lv et al. (73) |
| Adriamycin-induced CKD mice | ||||||
| Human samples | Patients with diabetic nephropathy | Increased levels of miR-19b-3p retrieved in uEVs samples | ||||
| miR-23a | In vitro | EVs from TECs under hypoxic conditions | Induction of macrophage switch to M1 phenotype and promotion of inflammation | Modulation of NF-κB cascade targeting ubiquitin editor A20 | Li et al. (74) | |
| In vivo | Injection of hypoxic-TEC-derived EVs in the renal parenchyma of mice | Increased number of inflammatory cells and higher mRNA levels of proinflammatory genes (TNF-α, IL-1β, and MCP-1) | ||||
| miR-150 | In vitro | Hypoxic proximal TECs | Upregulation of miR-150 expression, direct uptake by fibroblasts in culture | Guan et al. (75) | ||
| In vivo | Ischemia-injured mice | Increase of renal fibrosis | ||||
| miR-150-5p | In vitro | Hypoxic proximal TECs | Increased levels of miR-150-5p | Zhou et al. (76) | ||
| In vivo | Unilateral ischemia-reperfusion injury mice | Worsening of renal fibrosis | Inhibition of SOCS1 | |||
| miR-21 | In vitro | TGF-β1 stimulated TECs | Enrichment of miR-21 levels | Zhao et al. (77) | ||
| In vivo | Unilateral ureteral obstruction mouse model | Increased ECM deposition | Modulation of PTEN/AKT pathway | |||
| miR-221 | DKD | In vitro | High-glucose incubated podocyte-derived EVs | Dedifferentiation of proximal TECs | Modulation of Wnt/β-catenin signaling pathway targeting of DKK2 | Su et al. (78) |
| miR-25-3p | In vitro | Podocytes treated with M2 macrophage-derived EVs | Inhibition of apoptosis and EMT induced by high glucose treatment | Inhibition of DUSP1 expression and stimulation of apoptosis | Huang et al. (79) | |
| miR-145 | In vitro | TGF-β1-stimulated podocytes | Enrichment of miR-145 levels | Dimuccio et al. (80) | ||
| miR-126 | In vitro | TGF-β1-stimulated GECs | Reduction of miR-126 levels | Dimuccio et al. (80) |
The table summarizes the miRNAs involved in the progression of renal diseases. AKI, acute kidney injury; AKT, protein kinase B; CKD, chronic kidney disease; DKD, diabetic kidney disease; DKK2, Dickkopf-related protein 2; DUSP1, dual specificity protein phosphatase 1; ECM, extracellular matrix; EMT, epithelial-to-mesenchymal transition; EVs, extracellular vesicles; GECs, glomerular endothelial cells; IL-1β, interleukin 1β; LPS, lipopolysaccharide; MCP-1, monocyte chemoattractant protein 1; NF-κB, nuclear factor kappa light-chain enhancer of activated B cells; PTEN, phosphatase and tensin homolog; SOCS1, suppressor of cytokine signaling 1; TECs, tubular epithelial cells; TGF- β1, transforming growth factor β1; TNF-α, tumor necrosis factor α; uEV; Wnt, wingless-related integration site.