Table 1.
Changes of exosomal ncRNAs in diabetes.
| Source | Models | Contents | Alteration | Functions | References |
|---|---|---|---|---|---|
| adipose tissue macrophages | T2DM | miR-210 | increase | promoted diabetes pathogenesis by regulating glucose uptake and mitochondrial CIV activity | (15) |
| adipose tissue macrophage | T2DM | miR-29a | increase | induced insulin resistance | (16) |
| M1 macrophage | T2DM | miR-212-5p | increase | restricted insulin secretion | (17) |
| bone marrow-derived macrophages | T2DM | miR-144-5p | increase | impaired bone regeneration | (18) |
| macrophage | Diabetic vascular disease | miR-150-5p | decrease | promoted resistin expression in macrophages | (19) |
| M2 macrophages | Diabetic nephropathy | miR-93-5p | increase | attenuated LPS-induced podocyte apoptosis | (20) |
| EPCs | Diabetic wounds | miRNA-221-3p | increase | downregulated the expression of p27 and p57 proteins in the cell cycle signaling pathway | (21) |
| EPCs | Diabetic wounds | miR-126-3p | increase | promoted the recovery of tubulogenic function of high-glucose-impaired HUVECs. | (22) |
| EPCs | Diabetic stroke | miR-126 | increase | attenuated acute injury and promoted neurological function recovery | (23) |
| EPCs | Diabetic wounds | mmu_circ_0000250 | increase | enhanced the therapeutic effect of ADSC-exosomes to promote wound healing | (24) |
| ADSC | Diabetic wounds | miR-132 | increase | reduced inflammation, promoting angiogenesis and stimulated M2-macrophages polarization, promote wound healing | (25) |
| ADSC | Diabetic wounds | miR-21-5p | increase | induced M2 polarization of macrophages and augmented skin wound healing | (26) |
| HypADSCs | Diabetic wounds | miR-21-3p/miR-126-5p/miR-31-5p | increase | promoted diabetic wounds healing and inhibited inflammation | (27) |
| HypADSCs | Diabetic wounds | miR-99b/miR-146-a | decrease | promoted diabetic wounds healing and inhibited inflammation | (27) |
| MSCs | Diabetic kidney disease | miR-424-5p | increase | alleviated high glucose-induced cell apoptosis and EMT | (28) |
| MSCs | Diabetic kidney disease | miR-22-3p | increase | protected podocytes and reduced inflammation | (29) |
| MSCs | Diabetic nephropathy | miR-146a-5p | decrease | restored renal function, facilitated M2 macrophage polarization | (30) |
| MSCs | Retinal inflammation | miR-126 | decrease | reduced high glucose-induced HMGB1 expression and the activity of the NLRP3 inflammasome | (31) |
| MSCs | Diabetic wounds | miR -155 | increase | NA | (32) |
| MSCs | Diabetic foot ulcer | lncRNA H19 | decrease | prevented the apoptosis and inflammation of fibroblasts, leading to the stimulated wound-healing process | (33) |
| MSCs | Diabetic wound | lncRNA KLF3-AS1 | increase | down-regulated miR-383, boosted expression of VEGFA | (34) |
| MSCs | Diabetic stroke | miR-9 | decrease | promoted white matter remodeling and anti-inflammatory responses | (35) |
EPCs, endothelial progenitor cells; ADSC, adipocyte-derived stem cell; HypADSCs, hypoxia adipose stem cell; MSCs, mesenchymal stem cells; T2DM, type 2 diabetes mellitus; CIV,continuous intravenous infusion; LPS, lipopolysaccharide; HUVECs, human umbilical vein endothelial cells; EMT, epithelial-mesenchymal transition; HMGB1,high mobility group box 1 protein; NLRP3, nod-like receptor thermal protein domain associated protein 3; VEGFA, vascular endothelial growth factor A; NA, not applicable.