MTORC1 (Mechanistic Target of Rapamycin Complex 1) Signaling in Endothelial and Smooth Muscle Cells Is Required for Vascular Function.

ABSTRACT: mTORC1 (Mechanistic target of rapamycin complex 1) serves as a molecular hub and intracellular energy sensor that regulate various cellular processes. Emerging evidence points to mTORC1 signaling as a critical regulator of cardiovascular function with implications for cardiovascular disease. Here, we show that selective disruption of mTORC1, through conditional Raptor gene deletion, in endothelial or smooth muscle cells alter vascular function. Endothelial cell-specific Raptor deletion results in reduced relaxation responses evoked by acetylcholine in the aorta but not in the mesenteric artery. Of note, endothelial-specific Raptor deletion did not affect endothelial-independent vasorelaxation nor the contractile responses of the aorta or mesenteric artery. Interestingly, endothelial

SUBMITTER: Reho JJ 

PROVIDER: S-EPMC8678954 | biostudies-literature | 2021 Feb

REPOSITORIES: biostudies-literature