Figure 4 | Scientific Reports

Figure 4

From: Cardiomyocyte-specific deletion of GCN5L1 in mice restricts mitochondrial protein hyperacetylation in response to a high fat diet

Figure 4The alternative text for this image may have been generated using AI.

Impact of GCN5L1 deletion on ROS regulation and damage in response to a HFD. (A, B) Acetylation of superoxide dismutase 2 (SOD2) at K122 is significantly increased in whole cardiac tissue from WT animals in response to a HFD. There was no increase in SOD2 acetylation in GCN5L1 cKO mice under the same dietary conditions. (C) Cardiac lipid peroxidation in samples obtained from while cardiac tissue, a measure of ROS damage, is significantly lower in GCN5L1 cKO mice relative to WT mice under HFD conditions. Values are expressed as means ± SD, n = 4–8, *P < 0.05 versus WT LFD, #P < 0.05 versus WT HFD.

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