Figure 7.

Schematic shows melatonin-induced resistance to oxidative stress (left), and how treatment with melatonin restored mitochondrial function by increasing the expression of HSPA1L and stabilizing parkin in hMSCs subjected to oxidative stress. Oxidative stress induces mitochondrial dysfunction by decreasing mitophagy, which results in accumulation of abnormal mitochondria. Melatonin-treated hMSCs increase their expression of HSPA1L, which stabilizes parkin-induced mitophagy and helps eliminate dysfunctional mitochondria; this cascade also increases mitochondrial membrane potential and decreases apoptosis in hMSCs placed under oxidative stress.