Fig. 1: CTRP3 overexpression alleviated TAC-induced mitochondrial dysfunction and oxidative stress injury. | Cell Death Discovery

Fig. 1: CTRP3 overexpression alleviated TAC-induced mitochondrial dysfunction and oxidative stress injury.

From: CTRP3 alleviates mitochondrial dysfunction and oxidative stress injury in pathological cardiac hypertrophy by activating UPRmt via the SIRT1/ATF5 axis

Fig. 1

A Left panel, representative electron microscope images of cardiomyocyte mitochondria. Right panel: Quantification of mitochondrial density and cristae/mitochondrial area in heart tissues (n = 5, 10–15 random fields were analyzed per sample). B Representative western blotting and quantification of OPA1, Cyt-b, MTCO1, and TOMM20 protein levels in heart tissues. GAPDH served as the loading control (n = 4). C Quantification of ATP levels in heart tissues (n = 5). D Left panel, representative fluorescence images of cardiac sections stained with DHE (red) to indicate ROS levels; nuclei were stained with DAPI (blue). Right panel, relative quantification of ROS fluorescence intensity in heart tissues (n = 6, 10–15 random fields were analyzed per sample). E Quantification of MDA levels in heart tissues (n = 10). F Quantification of SOD activity in heart tissues (n = 10). Data were analyzed by one-way ANOVA and represented as mean ± SEM. *P < 0.05; **P < 0.01; ***P < 0.001; ns not significant, MDA malondialdehyde, SOD superoxide dismutase, TAC transverse aortic constriction.

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