Renoprotective Effects of Aldose Reductase Inhibitor Epalrestat against High Glucose-Induced Cellular Injury

Figure 8

Diagram summarizing the deleterious effects of high glucose on renal tubular cells and the protective role of aldose reductase inhibition against high glucose-induced renal cell injury. Exposure to high glucose acutely activates Akt and ERK pathways in renal cells and causes mitochondrial membrane depolarization and ultimately results in renal cell injury and arrest of cells at G1 phase of cell cycle. Inhibition of aldose reductase via epalrestat reverses these effects (except for cell cycle arrest) and protects renal cells against high glucose-mediated toxicity. Δψm, relative mitochondrial membrane potential.