mTOR Contributes to Endothelium-Dependent Vasorelaxation by Promoting eNOS Expression and Preventing eNOS Uncoupling

Researchers showed that either the endothelium-specific deletion of Mtor to inhibit both mTOR complexes, or depletion of Raptor or Rictor to disrupt mTORC1 or mTORC2, caused impaired endothelial-dependent vasodilatation.