Fig. 4
From: SBK3 suppresses angiotensin II-induced cardiac hypertrophy by regulating mitochondrial metabolism
AAV9-SBK3 was beneficial for maintaining the morphology and function of mitochondria after Ang II administration in mice. (A) Representative images of mitochondrial transmission electron microscopy in cardiac tissue of each mouse group, scale bar = 500 nm. (B-G) Mitochondrial respiratory chain complex I–V (B: representative images of western blot, C: quantitative analysis), OPA1, Mfn1, Mfn2 (D: representative images, E: quantitative analysis), Drp1, p-Drp1 (F: representative images, G: quantitative analysis) were rebalanced after SBK3 overexpression in mice. NADH-Q oxidoreductase (complex I), succinate-Q oxidoreductase (complex II), UQ-cytochrome C oxidoreductase (complex III), ATP synthetase (complex V). n = 6 mice per group. The data were expressed as Mean ± SEM. *P < 0.05, **P < 0.01, ***p < 0.001, ns, non significant; one-way ANOVA test followed by the Newman–Keuls test.
