Table 2.

Roles of Sirtuin knockout (KO)/transgene (TG) on vascular homeostasis.

	Genetic Alteration	Cells Targeted	Vascular Phenotype	Ref.
SIRT1	KO	Endothelial cells	Promoted vascular aging with reduced muscle capillary, nephrosclerosis, and atherosclerosis	[119,120] [52,121]
	KO	Macrophages	Promoted Ang II-induced abdominal aortic aneurysm	[52]
	KO	VSMC	Promoted abdominal aortic aneurysm;	[48,53]
	TG	Endothelial cells	Inhibited hyperglycemia-induced endothelial dysfunction and atherosclerosis	[49,51]
	TG	VSMC	Inhibited abdominal aortic aneurysm, injury-induced neointima formation, and diet-induced aortic stiffness	[50,53,122]
SIRT3	KO	ALL	Spontaneous pulmonary arterial hypertension (PAH); PAH associated with HFpEF; promoted Ang II-induced hypertension and accelerated arterial thrombosis	[56,58,59,123,124]
	TG	ALL	Attenuated Ang II/deoxycorticosterone acetate-salt induced hypertension	[57]
SIRT5	KO	ALL	Blunted arterial thrombosis	[125]
	TG	ALL	Accelerated arterial thrombus formation	[125]
SIRT6	Heterozygote	ALL	Promoted atherosclerosis	[78,84]
	KO	Endothelial cells	Exacerbated hypertension and complications; enhanced atherosclerosis, stroke, and vascular aging.	[77,79,90,126]
	TG	VSMC	Reduced atherosclerosis	[88]
SIRT7	KO	ALL	Enhanced neointimal formation	[127]
	TG	VSMC	Attenuated neointimal formation	[127]
	TG	Endothelial cells	Extended lifespan in Hutchinson-Gilford progeria syndrome	[128]

KO, knockout; TG, transgene; VSMC, vascular smooth muscle cells; HFpEF, heart failure with preserved ejection fraction.