Table 2. Relationship between SIRT1 and pathophysiology on renal diseases.

Ace, acetylated; TG, transgenic; ↓, decreases; ↑, increases; ⊣, inhibits.

Animals, tissue, cells or SIRT1 activator	Target for SIRT1	Effect for pathophysiology of renal injuries	Reference(s)
Sirt1+/− mice	SIRT1↓ → Ace-HIF-2α (inactivation)↑	Erythropoetin↓	[50]
Medullary interstitial cells (Sirt1+/− mice)	SIRT1↓ → COX2↓ → PGE2↓	Oxidative stress, apoptosis and fibrosis in UUO↑	[64]
Resveratrol (proximal tubular cells)	SIRT1↑ → Ace-Smad3↓	Fibrosis in UUO↓	[65]
Resveratrol (proximal tubular cells)	SIRT1↑ → Ace-p53↓	Cisplatin-induced apoptosis↓	[68]
Proximal tubular cells (specific Sirt1-TG mice)	SIRT1↑ → Ace-FOXO3↓	Catalase↑, oxidative stress↓, peroxisome function↑ and cisplatin-induced renal injuries↓	[66,67]
Renal cortex (Wistar fatty rats)	SIRT1↓ → Ace-NF-κB (p65)↑	Inflammation in diabetic nephropathy↑	[79]
Proximal tubular cells (Sirt1+/− mice) (aging mice)	SIRT1↓ → Ace-FOXO3a↑	Autophagy↓, abnormal mitochondria↑ and aging kidney ↑	[46]
Mesangial cells	SIRT1⊣ Ace-p53	Oxidative stress-induced apoptosis↓	[47]
Mesangial cells	SIRT1⊣ Ace-Smad 7	TGF-β-induced apoptosis↓	[82]
Podocytes	SIRT1⊣ Ace-FOXO4	AGE-induced apoptosis↓	[83]
Endothelial cells	SIRT1⊣ Ace-eNOS	NO↑	[85]
Collecting duct cells	SIRT1⊣ ENaC α-subunit	Na+ reabsorption↓	[94]