Focal Adhesion Kinase Drives Rho/ROCK and mTOR Signaling to Protect and Augment Aortic Dissections
Dysfunctional mechanosensing via focal adhesions (FAs) significantly contributes to thoracic aortic dissection in the beta-aminopropionitrile mouse model by triggering focal adhesion kinase (FAK) activation and subsequent Rho/ROCK and mTOR signaling pathways. The present findings indicate that these signaling pathways play distinct roles in ascending versus descending dissections. Specifically, in the ascending aorta, smooth muscle cell FAK-Rho/ROCK signaling acts as a beneficial adaptive mechanism to prevent dissections, whereas mTOR signaling is pathogenic and contributes to dissections.