Mitochondria are dynamic organelles that constantly undergo fission, fusion and mitophagy to facilitate mitochondrial quality control, which is crucial for maintaining vascular homeostasis.However, the underling mechanism in regulating mitochondrial quality remains to be elucidated.Sirtuin3 (SIRT3) is the major mitochondria NAD (+)-dependent deacetylase that regulates mitochondrial integrity and metabolism.We have previously shown that elevated blood pressure might accelerate age-related vascular remodelling and dysfunction; these changes were associated with reduced level of SIRT3 and altered mitochondrial dynamics.The current study was designed to investigate the effects of SIRT3 deficiency during angiotensin Ⅱ (Ang Ⅱ) induced vascular aging process.Chronic Ang Ⅱ infusion resulted in endothelial dysfunction in wildtype (WT) mice, which was particularly aggravated in SIRT3 knockout (SIRT3-/-) mice.In parallel, SIRT3 deficiency accelerated Ang Ⅱ-elevated senescence-associated β-galactosidase activity and the expression of cyclin-dependent kinase inhibitor 2A (p16INK4) and checkpoint homologs 2 (Chk-2) in aortic rings.Moreover, SIRT3-/-mice exposed to Ang Ⅱ also exhibited increased mitochondrial oxidative stress and reduced activities of endogenous antioxidant enzymes,associated with significantly reduced mitochondrial biogenesis and autophagy.In murine endothelial cells SIRT3 over-expression suppressed Angll-induced cellular senescence, alleviated mitochondrial reactive oxygen species generation, and restored the impaired mitochondrial quality control.Taken together, our results indicate that SIRT3 as a key regulator of mitochondrial quality control may contribute to vascular aging.