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. Author manuscript; available in PMC: 2022 May 1.
Published in final edited form as: J Mol Cell Cardiol. 2020 Dec 27;154:80–91. doi: 10.1016/j.yjmcc.2020.12.013

Fig. 7. Schematic graph of the mechanism by which the sEH gene regulates lipotoxic cardiomyopathy.

Fig. 7

Upper panel shows that HFD led to mouse obesity and lipotoxic cardiomyopathy. These can be attenuated by sEH gene deficiency. Lower panel demonstrates that sEH gene deletion increases EETs, EETs promote AMPK phosphorylation and activates AMPK, activated AMPK decreases mTORC phosphorylation and suppresses mTORC, and suppressed mTORC increases lipid autophagy. This reaction chain finally leads to attenuation of lipotoxic cardiomyopathy resulting from lipid accumulation.