Skip to main content
. 2021 Jun 18;45:102049. doi: 10.1016/j.redox.2021.102049

Fig. 2.

Fig. 2

Loss of FUNDC1-associated mitophagy promotes cardiomyocyte death and mitochondrial dysfunction. The AC16 human ventricular cardiomyocyte cell line was treated with 10 μg/mL of LPS to induce sepsis-related cardiomyocyte damage. UA, an inducer of mitophagy, was used to culture AC16 cells. siRNA against FUNDC1 (si-FUNDC1) was transfected into AC15 to inhibit mitophagy activation. A. Cell viability was determined using an MTT assay. B. ELISA analysis of caspase-3 activity. C-D. AC16 cells were stained with JC-1 to observe changes in the mitochondrial membrane potential. E-F. AC16 cells were stained with the MitoSOX red mitochondrial superoxide indicator to show changes in mitochondrial ROS. G. Total ATP production was determined using the Cell Titer-Glo Luminescent Viability assay. H-J. Mitochondrial morphology was revealed using confocal immunofluorescence. TOM20 was used to show the shape of mitochondria in response to LPS or FUNDC1 deletion. Data are presented as mean ± SEM, normalized per 1000 cardiomyocytes. *P<0.05. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)