Fig. 5

HG-induced mitochondrial dysfunction is restrained by overexpression of YME1L and accelerated by silencing of YME1L in HK2 cells. A TEM images of mitochondrial morphology in each group. Scale bar: 2 µm. B–E The intracellular ROS production was measured via flow cytometry in HK2 cells transfected YME1L-plasmid, si-YME1L, and their corresponding controls on stimulation with D-glucose for 48 h (n = 3). F–I Mitochondrial ROS in HK2 cells transfected YME1L-plasmid, si-YME1L, and their corresponding controls were analyzed by confocal microscopy after staining with MitoSOX. D-glucose was added 48 h before staining (n = 4). Scale bar: 50 µm. J, K ATP levels were detected via luciferase assay in HK2 cells transfected YME1L-plasmid, si-YME1L, and their corresponding controls on stimulation with D-glucose for 48 h (n = 3). Data are shown as mean ± SD. *p < 0.05, **p < 0.01, ***p < 0.001