Fig. 3
From: SBK3 suppresses angiotensin II-induced cardiac hypertrophy by regulating mitochondrial metabolism
Overexpression of SBK3 via the AAV9 vector suppressed Ang II-induced cardiac hypertrophy in mice. (A, B) AAV9-SBK3 decreased the left ventricular posterior wall thickness at systole (LVPW;S), left ventricular posterior wall thickness at diastole (LVPW; D), interventricular septal thickening at systole (IVS;S) and interventricular septal thickening at diastole (IVS; D) in mice induced by Ang II (1000 ng/kg/min), as determined by M-mode echocardiography. (C) Representative images of mouse heart in each group (scale bar = 1 mm), (G-J) AAV9-SBK3 reduced the HW/BW, LVWBW (D), cross-sectional area of cardiomyocytes (E and F, scale bar = 50 μm) and mRNA expression of ANP, BNP (G) altered by Ang II (1000 ng/kg/min) in mice. (K–N) The area of Masson’s trichrome (H and I, scale bar = 50 μm) and the LDH (J), CK (K) levels decreased after AAV9-SBK3 injection; 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.
