srt3025 has been researched along with Renal-Insufficiency--Chronic* in 2 studies
2 other study(ies) available for srt3025 and Renal-Insufficiency--Chronic
| Article | Year |
|---|---|
Late intervention in the remnant kidney model attenuates proteinuria but not glomerular filtration rate decline.
The use of animal models to predict the response to new therapies in humans is a vexing issue in nephrology. Unlike patients with chronic kidney disease (CKD), few rodent models develop a progressive decline in glomerular filtration rate (GFR) so that experimental studies frequently report a reduction in proteinuria as the primary efficacy outcome. Moreover, while humans present with established kidney disease that continues to progress, many experimental studies investigate therapies in the prevention rather than in a therapeutic setting.. We used the remnant kidney (subtotal nephrectomy [SNX]) rat model that develops a decline in GFR in conjunction with heavy proteinuria and hypertension along with the histological hallmarks of CKD in humans, glomerulosclerosis and tubulointerstitial fibrosis. Using agents that had been shown to improve GFR as well as proteinuria in the prevention setting, angiotensin-converting enzyme (ACE) inhibition with enalapril and SIRT1 activation with SRT3025, treatment was initiated 6 weeks after SNX.. While enalapril reduced blood pressure, proteinuria and histological injury, it did not improve GFR, as measured by inulin clearance. SRT3025 improved neither GFR nor structural damage despite a reduction in proteinuria.. These findings demonstrate that neither a reduction in proteinuria nor a reversal of structural damage in the kidney will necessarily translate to a restoration of kidney function. Topics: Angiotensin-Converting Enzyme Inhibitors; Anilides; Animals; Disease Models, Animal; Disease Progression; Enalapril; Glomerular Filtration Rate; Hypertension; Kidney; Nephrectomy; Postoperative Complications; Proteinuria; Rats; Renal Insufficiency, Chronic; Sirtuin 1; Thiazoles | 2021 |
Sirtuin 1 Activation Reduces Transforming Growth Factor-β1-Induced Fibrogenesis and Affords Organ Protection in a Model of Progressive, Experimental Kidney and Associated Cardiac Disease.
Topics: Acetylation; Anilides; Animals; Biopsy; Blood Pressure; Collagen; Disease Models, Animal; Disease Progression; Feeding Behavior; Fibrosis; Gene Expression Regulation; Genes, Reporter; Glomerulosclerosis, Focal Segmental; Heart Diseases; Heart Function Tests; HEK293 Cells; Humans; Kidney; Kidney Diseases; Kidney Function Tests; Proline; Rats, Inbred F344; Renal Insufficiency, Chronic; RNA, Messenger; Sirtuin 1; Smad3 Protein; Thiazoles; Transforming Growth Factor beta1 | 2017 |