| Small RNA |
| miR-150 |
Renal tubular epithelial cells, endothelial cells |
c-MYB (direct), IGF1R (indirect) |
AKI |
Slight diminution during AKI |
Genetic ablation conferred protection against AKI; treatment modality not tested |
[69] |
| miR-24 |
Renal tubular epithelial cells, endothelial cells |
HMOX1 (direct), H2AX (direct) |
AKI |
Increased during AKI |
Antagonism using LNA; preventative administration conferred protection against AKI in a mouse model |
[70] |
| miR-21 |
Renal tubular epithelial cells |
PTEN (direct), AKT phosphorylation (indirect) |
AKI |
Increased during AKI; mediator of Xenon preconditioning effect |
Exogenous administration might confer protection against AKI; not tested in in vivo models
|
[72] |
| miR-687 |
Renal tubular epithelial cells |
PTEN (direct) |
AKI |
Increased during AKI |
Blockade using anti-miR LNA conferred protection during preventative regimen in mouse model of AKI |
[73] |
| miR-494 |
Renal tubular epithelial cells |
ATF3 (direct) |
AKI |
Increased during AKI |
Blockade using lentiviral mediated anti-miR administration conferred renoprotection in a mouse model of AKI
|
[71] |
| miR-382 |
Renal tubular epithelial cells |
Kallikrein 5 |
CKD |
Increased during kidney fibrosis |
Antagonism using LNA conferred protection against fibrosis in a mouse model; preventative treatment |
[137] |
| miR-21 |
Inflammatory macrophages, pericytes |
PPARa |
CKD |
Increased during kidney fibrosis |
Antagonism using LNA conferred protection against fibrosis in a mouse model |
[39] |
| miR-29 |
Mesangial cells, Podocytes |
COLLI and COLLIV
|
CKD |
Decreased during kidney fibrosis; renoprotective agents, such as ROCK inhibitor, restored levels of miR-29 |
Supplementation could prove beneficial; untested potential |
[44] |
| miR-192 |
Mesangial cells |
ZEB1/2 |
DN |
Increased during DN |
LNA-mediated antagonism alleviated proteinuria in mouse models |
[138] |
| miR-23b |
Renal tubular epithelial cells |
G3BP2 |
DN |
Decreased in diabetic milieu |
Exogenous supplementation of miR-23b or silencing of G3BP2 in diabetic mice alleviated features of fibrosis and albuminuria; similarly, administration of miR-23b antagomiR promoted renal fibrosis in healthy mice |
[139] |
| miR-17∼92 |
Renal tubular epithelial cells |
PKD1, PKD2, HNF1b, PKHD1 |
PKD |
Increased in cystic kidneys |
Genetic deletion suppressed cyst growth |
[140] |
| miR-21 |
Renal tubular epithelial cells |
PDCD4 |
PKD |
Increased in cystic kidneys |
Genetic deletion suppressed cyst growth |
[141] |
| miR-148b |
Peripheral blood mononuclear cells |
C1GALT1 (core 1,β1,3-galactosyltransferase 1) |
IgAN |
Increased in PBMCs from patients with IgAN |
Untested potential applications include reconstitution of miR-148b-silenced PBMCs/bone marrow chimeras during early stages of disease |
[142] |
| Long ncRNA |
| lnc-MGC |
Podocytes |
ATF3, CUGBP2, PUM2, TNRC6B, HuR, PTEN |
DN |
Increased in diabetic milieu |
LNA-mediated silencing of lnc-MGC ameliorated pathobiological features |
[86] |
| Tug1 |
Podocytes |
PGC1a pathway |
DN |
Decreased in diabetic milieu |
Untested potential applications include supplementation of Tug1 |
[87] |
