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. 2016 Jul 25;7(14):290–301. doi: 10.4239/wjd.v7.i14.290

Table 2.

In vitro and in vivo renal cell models demonstrating the potential involvement of miRNAs in development of diabetic kidney disease

miRNA Species Specimen miRNA expression Mechanism of action Ref.
miR-192 Mice/Rat M, Te, KT Inconsistent results Interaction with TGFβ-associated and other pro-fibrotic genes [94-96]
Human Te, KT Reduced [97]
miR-216a Mice M, KT Elevated [98]
miR-377 Mice M, KT Elevated [99]
Human M
miR-29c Mice P, KT Elevated [100]
miR-200b/c Mice M, KT Elevated [101]
miR-21 Mice KT Elevated [102]
Human Te
miR-1207-5p Human P, M, Te Elevated [103]
miR-200a Rat Te Reduced [104]
Mice KT
miR-23b Mice KT Reduced [105]
Human Te, HEK-293A
miR-93 Mice P, En, KT Reduced Regulation of VEGF expression [106]
miR-25 Rat M, KT Reduced Regulation of NOX4 expression [107]
miR-451 Mice M, KT Reduced Targeting YwhaZ and p38 MAPK signaling pathways [108]

M: Mesangial cells; Te: Tubular epithelial cells; KT: Kidney tissue; P: Podocytes; En: Endothelial cells; TGFβ: Transforming growth factor β; VEGF: Vascular endothelial growth factor; NOX4: Nicotinamide adenine dinucleotide phosphate hydrogen oxidase 4; YwhaZ: Tyrosine3-monooxygenase/tryptophan 5-monooxygenase activation protein, zeta; MAPK: Mitogen-activated protein kinase; HEK-293A: Human Embryonic Kidney-293A cells.