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Background  Emerging evidence indicates that impaired angiogenesis may contribute to hypertension‐induced cardiac remodeling. The nicotinamide adenine dinucleotide–dependent deacetylase Sirtuin 3 ( SIRT 3) has the potential to modulate angiogenesis, but this has not been confirmed. As such, the aim of this study was to examine the relationship between  SIRT 3‐mediated angiogenesis and cardiac remodeling.    Methods and Results  Our experiments were performed on  SIRT 3 knockout and age‐matched wild‐type mice infused with angiotensin  II  (1400 ng/kg per minute) or saline for 14 days. After angiotensin  II  infusion,  SIRT 3 knockout mice developed more severe microvascular rarefaction and functional hypoxia in cardiac tissues compared with wild‐type mice. These events were concomitant with mitochondrial dysfunction and enhanced collagen I and collagen  III  expression, leading to cardiac fibrosis. Silencing  SIRT 3 facilitated angiotensin  II –induced aberrant Pink/Parkin acetylation and impaired mitophagy, while excessive mitochondrial reactive oxygen species generation limited angiogenic capacity in primary mouse cardiac microvascular endothelial cells. Moreover,  SIRT 3 overexpression in cardiac microvascular endothelial cells enhanced Pink/Parkin‐mediated mitophagy, attenuated mitochondrial reactive oxygen species generation, and restored vessel sprouting and tube formation. In parallel, endothelial cell–specific  SIRT 3 transgenic mice showed decreased fibrosis, as well as improved cardiac function and microvascular network, compared with wild‐type mice with similar stimuli.    Conclusions  Collectively, these findings suggest that  SIRT 3 could promote angiogenesis through attenuating mitochondrial dysfunction caused by defective mitophagy.

Sirtuin 3 Deficiency Accelerates Hypertensive Cardiac Remodeling by Impairing Angiogenesis