Dataset related to: Sirtuin 3 Deficiency Aggravates Kidney Disease in Response to High-Fat Diet through Lipotoxicity-Induced Mitochondrial Damage

The files contain all the dataset included in the manuscript divided by figures. Abstract: Sirtuin 3 (SIRT3) is the primary mitochondrial deacetylase that controls the antioxidantpathway and energy metabolism. We previously found that renal Sirt3 expression and activity werereduced in mice with type 2 diabetic nephropathy associated with oxidative stress and mitochondrialabnormalities and that a specific SIRT3 activator improved renal damage. SIRT3 is modulated bydiet, and to assess whether Sirt3 deficiency aggravates mitochondrial damage and accelerates kidneydisease in response to nutrient overloads, wild-type (WT) and Sirt3-/- mice were fed a high-fat-diet(HFD) or standard diet for 8 months. Sirt3-/- mice on HFD exhibited earlier and more severealbuminuria compared to WT mice, accompanied by podocyte dysfunction and glomerular capillaryrarefaction. Mesangial matrix expansion, tubular vacuolization and inflammation, associated withenhanced lipid accumulation, were more evident in Sirt3-/- mice. After HFD, kidneys from Sirt3-/-mice showed more oxidative stress than WT mice, mitochondria ultrastructural damage in tubularcells, and a reduction in mitochondrial mass and energy production. Our data demonstrate that Sirt3deficiency renders mice more prone to developing oxidative stress and mitochondrial abnormalitiesin response to HFD, resulting in more severe kidney diseases, and this suggests that mitochondriaprotection may be a method to prevent HFD-induced renal injury.