Fig. 8: Schematic illustrating the regulation of NO bioavailability and EDD function by mTOR signaling. | Communications Biology

Fig. 8: Schematic illustrating the regulation of NO bioavailability and EDD function by mTOR signaling.

From: mTOR contributes to endothelium-dependent vasorelaxation by promoting eNOS expression and preventing eNOS uncoupling

Fig. 8

Inhibition of mTORC1 suppresses eNOS gene expression, by impairing p70S6K-mediated posttranscriptional regulation of the transcription factor KLF2 expression. In contrast to mTORC1 inhibition, targeting mTORC2 does not affect eNOS expression. Rather, disruption of mTORC2 results in activation of MAPK (p38 and JNK), which are normally suppressed. A positive-feedback loop with Nox2 upregulation is enabled that contributes to the excessive generation of reactive oxygen species (ROS), leading to eNOS uncoupling and decreased NO bioavailability in mTORC2-inhibited EC.

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