Endothelial mTOR operates as a metabolic dial that shifts cells between collective tissue functions and solitary survival programs. We hypothesize that the NAD+-dependent deacetylase SIRT1 sets the position of this dial by directly deacetylating mTORC1 regulatory proteins, thereby coupling cellular redox state to the mTOR-driven senescence-survival trade-off. When NAD+ levels fall with age, SIRT1 activity declines, leading to hyperacetylation of Raptor and mTOR, which sensitizes mTORC1 to amino-acid signals and locks the endothelium in a pro-growth, SASP-prone state. Conversely, boosting NAD+ restores SIRT1 deacetylase activity, attenuating mTORC1 signaling without abolishing it, thereby lowering mitochondrial ROS, recoupling eNOS, and suppressing ICAM-1-mediated inflammation while preserving enough anabolic capacity for angiogenic repair. To test this, we propose three complementary experiments in aged mouse aortas and human umbilical vein endothelial cells (HUVECs) exposed to chronic TNF-alpha. First, endothelial-specific SIRT1 overexpression via AAV9 will be compared to global mTORC1 inhibition with rapalink-1. We predict that SIRT1 overexpression will reduce p-S6K1 levels by ~40% (vs ~70% with rapalink-1), decrease mitochondrial ROS by 35%, increase NO bioavailability by 45%, and cut ICAM-1 expression by 50%, matching the functional improvements seen with partial mTORC1 inhibition. Second, we will measure acetylation of Raptor (Lys749) and mTOR (Ser2448) by immunoprecipitation followed by Western blot; SIRT1 overexpression should lower acetylation at these sites, an effect blocked by the SIRT1 inhibitor EX-527. Third, functional angiogenesis will be assessed using Matrigel tube formation and ex vivo aortic ring assays. We anticipate that SIRT1-enhanced endothelia will retain 80% of the tube-length capacity of young controls, whereas rapalink-1-treated cells will drop to 50%, indicating that excessive mTORC1 suppression impairs repair capacity. A falsifiable outcome would be that SIRT1 overexpression fails to reduce p-S6K1 or ROS when NAD+ is simultaneously depleted by CD38 over-expression, confirming that the SIRT1-mTOR axis depends on NAD+ flux. Additionally, if mTORC2-Akt signaling remains unchanged across conditions, the observed benefits can be attributed to selective mTORC1 tuning rather than global mTOR shutdown. By positioning SIRT1 as a NAD+-sensitive rheostat that fine-tunes mTORC1 activity, this hypothesis extends the civilization-versus-survival dial concept: optimal endothelial health does not require abandoning the collective program but rather adjusting its intensity to match metabolic availability. Interventions that raise NAD+ (e.g., NR, NMN) or activate SIRT1 (e.g., SRT1720) could thus achieve the same vascular benefits as rapalogs while preserving the anabolic reserve needed for endothelial regeneration.