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Table 2 miRNAs involved in diabetes-related renal inflammation and fibrogenesis

From: Effects of metabolic memory on inflammation and fibrosis associated with diabetic kidney disease: an epigenetic perspective

Types

Functions involved

miRNAs

Expression

levels

Target genes

Mechanisms

Ref

T1DN-related miRNAs

Renal Inflammation

miR-21

Upregulation

TIMP3

upregulation of miR-21 enhanced the excretion of pro-inflammatory factors by repressing the expression of TIMP3

[96]

miR-146a

Upregulation

IRAK1/TRAF6

upregulation of miR-146a promoted NF-kB mediated upregulation of pro-inflammatory cytokines by negative feedback to Irak1 and Traf6

[97]

miR-146a

Downregulation

Nox4

miR‑146a/Nox4 decreases ROS generation and inflammation and prevents DN

[98]

Renal Fibrosis

miR-192

Upregulation

GLP1R

upregulation of miR-192 exerted its pro-fibrotic effects by directly targeting GLP1R

[99, 100]

miR-214

Upregulation

PTEN

upregulation of miR-214 contributed to renal cell hypertrophy and matrix protein expression by directly acting on PTEN

[101]

miR-22

Upregulation

PTEN

upregulation of miR-22 promoted renal tubulointerstitial fibrosis by suppressing autophagy partially via targeting PTEN

[102]

miR-382

Upregulation

FOXO1

upregulation of miR-382-induced glomerular mesangial cell proliferation and ECM accumulation by targeting FOXO1

[103]

miR-137

Downregulation

Notch1

miR-137 inhibition aggravated ECM protein accumulation via directly targeting Notch1

[104]

Both inflammation and fibrosis

miR-455-3p

Downregulation

ROCK2

downregulated miR-455-3p aggravated the progression of renal inflammation and fibrosis through promoting ROCK2 expression

[105]

T2DN related miRNAs

Renal Inflammation

miR-146a

Upregulation

IRAK1/TRAF6

upregulation of miR-146a promoted NF-kB mediated upregulation of pro-inflammatory cytokines by negative feedback to Irak1 and Traf6

[97]

Renal Fibrosis

miR-133b/199b

Upregulation

Sirt 1

upregulation of miR-133b and miR-199b enhanced TGF-β1-induced epithelial to mesenchymal transition and renal fibrosis by targeting SIRT1 in diabetic nephropathy

[107]

miR-23a

Upregulation

SnoN

upregulation of miR-23a promoted high glucose-induced EMT and renal fibrogenesis by down-regulation of SnoN

[112]

miR-30e

Downregulation

GLIPR-2

miR-30e inhibited GLIPR-2 and then promoted the proliferation of RTECs and inhibited EMT, ultimately leading to renal fibrosis in DN

[109]

miR-93

Downregulation

Orai1

downregulation of microRNA-93-induced TGF-b1-induced EMT and renal fibrogenesis by down-regulation of Orai1

[110]

Both inflammation and fibrosis

miR-29b

Downregulation

SP1/Smad-3/NF-κB

miR-29b played a protective role in diabetic kidney disease by the inhibition of Sp1 expression, TGF-β/Smad3-dependent renal fibrosis, and NF-κB-driven renal inflammation

[106]

Renal Inflammation

miR-423-5p

Downregulation

Nox4

miR-423-5p suppressed high-glucose induced podocyte injury and inhibited ROS generation by targeting Nox4

[95]

Not mentioned

Renal Fibrosis

miR-4490

Upregulation

PSMA6

upregulation of miRNA-4490 regulated PSMA6 mRNA level post-transcriptionally

[94]

miR-326-3p

Downregulation

FcγRIII

miR-326-3p ameliorates high glucose and ox-LDL-IC-induced fibrotic injury in renal mesangial cells by targeting FcγRIII

[113]

Both inflammation and fibrosis

miR-199a-5p

Upregulation

Klotho

upregulated expression of miR-199a-5p decreased Klotho expression, resulting in activating the TLR4/NF-kB p65/NGAL signaling pathways and the downstream fibrosis and inflammation in HG-induced rat mesangial cells

[108]