Figure 5.

Schematic representing the interplay between ET-1/ET_A/ET_B receptor and mTOR signaling under HG conditions in H9c2 cells. HG treatment leads to increased production of ROS, mitochondrial damage, decreased expression of survival markers, and increased expression of apoptosis markers. These HG-induced cardiomyocyte damages were ameliorated by inhibition of endothelin receptors ET_A-R alone, both ET_A-R/ET_B-R, or partial suppression of mTOR complex. HG: High glucose; ROS: Reactive oxygen species; ET-1: Endothelin-1; siRap: silencing Raptor; siRic: silencing Rictor.