Fig. 5: CGI-58 knockout influences ER stress, oxidative stress, protein glycosylation, and fatty acid oxidation in the heart. | Cell Death & Disease

Fig. 5: CGI-58 knockout influences ER stress, oxidative stress, protein glycosylation, and fatty acid oxidation in the heart.

From: Cardiac-specific CGI-58 deficiency activates the ER stress pathway to promote heart failure in mice

Fig. 5

A–C CGI-58fl/fl and CGI-58cko mice were fed with ND for 3 months, and then the protein levels of GRP78, p-IRE, p-Elf2a, ATF6, CHOP, O-GlcNAc, protein carbonyls, Acaa2, and Hadh in the heart were examined. All statistical results are shown right, n = 4 per group. Data are presented as mean ± SEM, and n represents the number of samples or animals. *P < 0.05, **P < 0.01, ***P < 0.001.

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