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. Author manuscript; available in PMC: 2020 Apr 1.
Published in final edited form as: J Mol Cell Cardiol. 2019 Feb 15;129:69–78. doi: 10.1016/j.yjmcc.2019.02.009

Figure 8. Hypothesized mechanism of action by GCN5L1 in cardiac cells following I/R injury.

Figure 8.

Loss of GCN5L1 disrupts mitochondrial function leading to increased ROS production. Treatment of cells with antioxidants rescues GCN5L1-deficient cells after ischemic injury.