Fig. 8: Proposed mechanism by which MSCs prevent the progression of diabetic nephropathy.

a The M1 macrophage population is increased in diabetic kidneys, and pro-inflammatory cytokines suppress mitochondrial biogenesis to induce mitochondrial dysfunction in TECs. Increased ROS produced from dysfunctional mitochondria cause injury to TECs. In addition, diabetes may lead to the direct injury of TECs. TEC injury may in turn activate M1 macrophages to sustain the progression of diabetic nephropathy. b MSCs increase Arg1 expression in macrophages to suppress M1 macrophage polarization and prevent the deterioration of kidney function