Fig. 5.

PHB2 deficiency aggravated DOX-induced mitochondrial dysfunction in cardiomyocytes.

(A) Enzymatic activities of OXPHOS complex I–V in isolated mitochondria from primary cardiomyocytes with and without DOX challenge (0.1 μM) for 24 h after adenovirus transfection (n = 5 independent experiments per group). (B and C) OCR curves and quantification of basal respiration, maximal respiration, and ATP-coupled respiration in primary cardiomyocytes under various treatment settings (n = 6 independent experiments per group). (D and E) Representative images and quantification of fluorescence intensity of MitoSOX staining in adult mouse cardiomyocytes (AMCMs) under various treatment settings (n = 20 independent experiments per group). (F and G) Representative images and quantification of fluorescence intensity of TMRM staining in AMCMs under various treatment settings (n = 20–30 independent experiments per group). (H) ATP production in primary cardiomyocytes under various treatment settings (n = 6 independent experiments per group). (I) Measurement of cell viability using CCK-8 and CellTiter-Glo luminescent assay in primary cardiomyocytes under various treatment settings (n = 6 independent experiments per group). (J) LDH leakage in supernatants of primary cardiomyocytes under various treatment settings (n = 6 independent experiments per group). Mean ± SEM. *p < 0.05, **p < 0.01, ****p < 0.0001, ns, no significance. For statistical analysis, two-way ANOVA with Tukey's test for multiple comparisons was used.