Table 1 Role of exosomes in treatment of DN
From: Role of exosomes in pathogenesis, diagnosis, and treatment of diabetic nephropathy
Source of exosomes | Model | Cargo | Action | Ref |
|---|---|---|---|---|
M2 macrophages | Mouse podocyte cell line | miR-25-3p | Inhibit expression of DUSP, activating podocyte autophagy and attenuating podocyte apoptosis | [51] |
PTECs | STZ-induced DN mice | miR-26a-5p | Bind CHAC1, inhibiting the CHAC1/NF-κB pathway, thus inhibits the inflammatory response. The expression of miR-26a-5p in exosomes is increased by inhibiting Rab27a. | [52] |
ADSCs | Mouse podocyte cell line | miRNA-215-5p | Attenuate epithelial–mesenchymal transition (EMT) by inhibiting the transcription of ZEB2, thus reducing podocyte loss | [53] |
ADSCs | db/db mice | miR-486 | Enhance autophagy and reduce apoptosis of MPCs by inhibiting the Smad1/mTOR signaling pathway in podocytes | [54] |
ADMSCs | Rat glomerular mesangial cell line, STZ-induced DN Sprague–Dawley rat | miR-125a | Inhibit apoptosis and protect against DN by modulating histone deacetylase-1 (HDAC1) and downregulating endothelin-1 (ET-1) | [55] |
MSCs | db/db mice | miR- 424-5p | Inhibit YAP1 activation, thus reducing high glucose- induced apoptosis and reduced EMT. It attenuates DKD progression | [56] |
MSCs | Human embryonic kidney epithelial cells (HKCs) injury induced by high glucose (HG) | miR-125b | Induce autophagy and inhibit apoptosis by downregulating TRAF6/Akt signaling pathway | [57] |
MSCs | STZ-induced DN albino rats | ……….. | Induce autophagy and suppression the mTOR pathway, leading to improved renal function and histological restoration of renal tissues | [58] |
HUC-MSCs | Podocyte cell line and mice | miR-22-3p | Ameliorate kidney injury by reducing inflammation in podocytes and inhibiting the activation of NLRP3 signaling pathway in podocytes | [59] |
HUC-MSCs | STZ-induced DN rats | miR-146a-5p | Inhibit TRAF6/STAT1signaling pathway, thus mediate macrophage shifting polarization from M1 to M2. Reduce inflammatory cytokine level | [60] |
HUC-MSCs | STZ-induced DN rats, renal tubular epithelial cell lines (NRK-52E, HK2), and human renal glomerular endothelial cell line (hrGECs). | ……….. | Reducing pro-inflammatory cytokines (IL-6, IL-1β, and TNF-α) and pro-fibrotic factor (TGF-β), thus inhibit renal interstitial inflammation, fibrosis, improve renal function, and prevent progression of DN | [61] |
BMMSC | STZ-induced DN Sprague–Dawley rat | ……….. | Inhibit JAK2/STAT3 expression, therefore attenuate renal tissue damage in DN patients and improve renal function | [62] |
urinary exosomes | STZ-induced DN rats | miR-30, miR-let-7 family, miR-24-3p, miR-23a-3p | Compensate for the loss of protective miRNAs, so provide a reno-protective effect | [63] |
USCs-Exo | STZ-induced DN Sprague–Dawley rat model Human podocytes cell line | GFs, angiogenin, BMP-7 | Reduce urinary microalbumin excretion, inhibit apoptosis, suppress the caspase-3 overexpression. In vitro, reduce podocyte apoptosis | [64] |
USCs-Exo | Human podocytes cell line STZ-induced DN Sprague–Dawley rat model | miR-16-5p | improve podocyte injury by compensate the inhibited miR-16–5p due to high glucose and silencing VEGFA | [65] |