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8 results for “Sirtuin 3”
Dataset related to: Low Nephron Number Induced by Maternal Protein Restriction Is Prevented by Nicotinamide Riboside Supplementation Depending on Sirtuin 3 Activation
<p>The files contain all the dataset included in the manuscript divided by figures. For each figure, individual tabs indicate data from different figure panels.</p> <p> </p> <p><strong>Abstract</strong></p> <p>A reduced nephron number at birth, due to critical gestational conditions, including maternal malnutrition, is associated with the risk of developing hypertension and chronic kidney disease in adulthood. No interventions are currently available to augment nephron number. We have recently shown that sirtuin 3 (SIRT3) has an important role in dictating proper nephron endowment. The present study explored whether SIRT3 stimulation, by means of supplementation with nicotinamide riboside (NR), a precursor of the SIRT3 co-substrate nicotinamide adenine dinucleotide (NAD<sup>+</sup>), was able to improve nephron number in a murine model of a low protein (LP) diet. Our findings show that reduced nephron number in newborn mice (day 1) born to mothers fed a LP diet was associated with impaired renal SIRT3 expression, which was restored through supplementation with NR. Glomerular podocyte density, as well as the rarefaction of renal capillaries, also improved through NR administration. In mechanistic terms, the restoration of SIRT3 expression through NR was mediated by the induction of proliferator-activated receptor γ (PPARγ) coactivator-1α (PGC-1α). Moreover, NR restored SIRT3 activity, as shown by the reduction of the acetylation of optic atrophy 1 (OPA1) and superoxide dismutase 2 (SOD2), which resulted in improved mitochondrial morphology and protection against oxidative damage in mice born to mothers fed the LP diet. Our results provide evidence that it is feasible to prevent nephron mass shortage at birth through SIRT3 boosting during nephrogenesis, thus providing a therapeutic option to possibly limit the long-term sequelae of reduced nephron number in adulthood.</p>
Dataset related to: Sirtuin 3 Deficiency Aggravates Kidney Disease in Response to High-Fat Diet through Lipotoxicity-Induced Mitochondrial Damage
<p>The files contain all the dataset included in the manuscript divided by figures.</p> <p> </p> <p>Abstract: Sirtuin 3 (SIRT3) is the primary mitochondrial deacetylase that controls the antioxidant<br>pathway and energy metabolism. We previously found that renal Sirt3 expression and activity were<br>reduced in mice with type 2 diabetic nephropathy associated with oxidative stress and mitochondrial<br>abnormalities and that a specific SIRT3 activator improved renal damage. SIRT3 is modulated by<br>diet, and to assess whether Sirt3 deficiency aggravates mitochondrial damage and accelerates kidney<br>disease in response to nutrient overloads, wild-type (WT) and Sirt3-/- mice were fed a high-fat-diet<br>(HFD) or standard diet for 8 months. Sirt3-/- mice on HFD exhibited earlier and more severe<br>albuminuria compared to WT mice, accompanied by podocyte dysfunction and glomerular capillary<br>rarefaction. Mesangial matrix expansion, tubular vacuolization and inflammation, associated with<br>enhanced lipid accumulation, were more evident in Sirt3-/- mice. After HFD, kidneys from Sirt3-/-<br>mice showed more oxidative stress than WT mice, mitochondria ultrastructural damage in tubular<br>cells, and a reduction in mitochondrial mass and energy production. Our data demonstrate that Sirt3<br>deficiency renders mice more prone to developing oxidative stress and mitochondrial abnormalities<br>in response to HFD, resulting in more severe kidney diseases, and this suggests that mitochondria<br>protection may be a method to prevent HFD-induced renal injury.</p>
Omega 3 Fatty Acids on Serum Irisin and Sirtuin-1 in Type 2 Diabetic Mellitus Patients Treated With Glimepiride
ClinicalTrials.gov study NCT03917940. IPD Sharing: NO. Countries: 1. Publications: 3.
Dataset related to article "Manipulating Sirtuin 3 pathway ameliorates renal damage in experimental diabetes"
<p><em>The files contain raw data related to the article "Manipulating Sirtuin 3 pathway ameliorates renal damage in experimental diabetes", available from <a href="https://www.nature.com/articles/s41598-020-65423-0">https://www.nature.com/articles/s41598-020-65423-0</a>.</em></p> <p><strong>Abstract of the manuscript</strong>: More effective treatments for diabetic nephropathy remain a major unmet clinical need. Increased oxidative stress is one of the most important pathological mechanisms that lead to kidney damage and functional impairment induced by diabetes. Sirtuin 3 (SIRT3) is the main mitochondrial deacetylase and critically regulates cellular reactive oxygen species (ROS) production and detoxification. Honokiol is a natural biphenolic compound that, by activating mitochondrial SIRT3, can carry out anti-oxidant, anti-inflammatory and anti-fibrotic activities. Here, we sought to investigate the renoprotective effects of honokiol in BTBR <em>ob/ob</em> mice with type 2 diabetes. Diabetic mice were treated with vehicle or honokiol between the ages of 8 and 14 weeks. Wild-type mice served as controls. Renal <em>Sirt3</em> expression was significantly reduced in BTBR <em>ob/ob</em> mice, and this was associated with a reduction in its activity and increased ROS levels. Selective activation of SIRT3 through honokiol administration translated into the attenuation of albuminuria, amelioration of glomerular damage, and a reduction in podocyte injury. SIRT3 activation preserved mitochondrial wellness through the activation of SOD2 and the restoration of PGC-1α expression in glomerular cells. Additionally, the protective role of SIRT3 in glomerular changes was associated with enhanced tubular <em>Sirt3</em> expression and upregulated renal <em>Nampt</em> levels, indicating a possible tubule-glomerulus retrograde interplay, which resulted in improved glomerular SIRT3 activity. Our results demonstrate the hitherto unknown renoprotective effect of SIRT3 against diabetic glomerular disease and suggest that the pharmacological modulation of SIRT3 activity is a possible novel approach to treating diabetic nephropathy.</p>
Nigral dopaminergic sirtuin 3 inhibits aging-related locomotor decline
GEO Series GSE246388. Mus musculus. 18 samples. Type: Expression profiling by high throughput sequencing.
Sirtuin 3 is a common target of non-steroidal anti-inflammatory drugs to induce gastric cancer cell death and gastric mucosal injury II.
GEO Series GSE202140. Homo sapiens. 6 samples. Type: Expression profiling by high throughput sequencing.
Sirtuin 3 and Sirtuin 7 in Systemic Sclerosis
ClinicalTrials.gov study NCT04303208. IPD Sharing: Not stated. Countries: 0. Publications: 0.
Sirtuin 3 is a common target of non-steroidal anti-inflammatory drugs to induce gastric cancer cell death and gastric mucosal injury.
GEO Series GSE201565. Rattus norvegicus. 10 samples. Type: Expression profiling by high throughput sequencing.
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International Brain Laboratory public data
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OpenNeuro
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