Fig. 6. Schematic representation of the proposed protective effect of melatonin treatment for mouse mesenchymal stem/stromal cells in chronic kidney disease (CKD-mMSCs) through modulating hexokinase-2 (HK2), thereby reducing the damage caused by the accumulation of methylglyoxal (MG) during abnormal or unscheduled glycolysis. In CKD-mMSCs, HK2 dissociates from the mitochondrial voltage-dependent anion channel (VDAC) and induces excessive production of a toxic glycolytic intermediate product (MG). This leads to mitochondrial dysfunction and impaired cell proliferation. Melatonin treatment of CKD-mMSCs enhances mitochondrial functions and rescues the normal expression of cell cycle-related proteins.
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