Figure 8.

A schematic diagram depicts molecular basis underlying DN treatment by hUSCs. The secretion of hUSC exosomes promoted the podocyte proliferation and inhibited the podocyte apoptosis to protect against HG‐induced podocyte injury, thereby alleviating the damage of diabetic nephropathy by down‐regulating VEGFA via exosomes carrying overexpressed miR‐16‐5p. DN, diabetic nephropathy; HG, high glucose; hUSCs, human urine‐derived stem cells; miR‐16‐5p, microRNA‐16‐5p; VEGFA, vascular endothelial growth factor A