Can we target tubular damage to prevent renal function decline in diabetes?
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Urinary Markers of Tubular Injury in Early Diabetic NephropathyImmune Cells and Inflammation in Diabetic NephropathyTipping the balance from angiogenesis to fibrosis in CKDMolecular mechanisms of diabetic kidney diseaseHigh glucose induces apoptosis via upregulation of Bim expression in proximal tubule epithelial cells.Renal tubular Sirt1 attenuates diabetic albuminuria by epigenetically suppressing Claudin-1 overexpression in podocytesThe proteasome inhibitor, MG132, attenuates diabetic nephropathy by inhibiting SnoN degradation in vivo and in vitro.Sonic hedgehog is a novel tubule-derived growth factor for interstitial fibroblasts after kidney injury.Endogenous fructose production and fructokinase activation mediate renal injury in diabetic nephropathy.Blocking ligand occupancy of the αVβ3 integrin inhibits the development of nephropathy in diabetic pigsTranscriptome analysis of proximal tubular cells (HK-2) exposed to urines of type 1 diabetes patients at risk of early progressive renal function decline.Urinary monocyte chemoattractant protein-1 and hepcidin and early diabetic nephropathy lesions in type 1 diabetes mellitus.Disruption of renal tubular mitochondrial quality control by Myo-inositol oxygenase in diabetic kidney disease.Sirtuin 1: A Target for Kidney Diseases.Mycophenolate mofetil ameliorates diabetic nephropathy through epithelial mesenchymal transition in ratsOxymatrine Inhibits Renal Tubular EMT Induced by High Glucose via Upregulation of SnoN and Inhibition of TGF-β1/Smad Signaling Pathway.Mouse chromosome 2 harbors genetic determinants of resistance to podocyte injury and renal tubulointerstitial fibrosis.SnoN upregulation ameliorates renal fibrosis in diabetic nephropathyAntioxidant diet and sex interact to regulate NOS isoform expression and glomerular mesangium proliferation in Zucker diabetic rat kidney.myo-Inositol Oxygenase Overexpression Accentuates Generation of Reactive Oxygen Species and Exacerbates Cellular Injury following High Glucose Ambience: A NEW MECHANISM RELEVANT TO THE PATHOGENESIS OF DIABETIC NEPHROPATHYTissue-specific metabolic reprogramming drives nutrient flux in diabetic complicationsThe mitochondria-targeted antioxidant MitoQ ameliorated tubular injury mediated by mitophagy in diabetic kidney disease via Nrf2/PINK1.Anti-diabetic effects of the Indian indigenous fruit Emblica officinalis Gaertn: active constituents and modes of action.Role of the potassium channel KCa3.1 in diabetic nephropathy.Targeting cellular drivers and counter-regulators of hyperglycaemia- and transforming growth factor-β1-associated profibrotic responses in diabetic kidney disease.Cell biology of diabetic nephropathy: Roles of endothelial cells, tubulointerstitial cells and podocytesKidney Injury Molecule-1 is Elevated in Nephropathy and Mediates Macrophage Activation via the Mapk Signalling Pathway.Insights into Diabetic Kidney Disease Using Urinary Proteomics and Bioinformatics.Tubular proteinuria is the dominant type of proteinuria in an elderly community population in China.Can existing drugs approved for other indications retard renal function decline in patients with type 1 diabetes and nephropathy?The ZDSD rat: a novel model of diabetic nephropathy.Potassium channels, renal fibrosis, and diabetes.A molecular morphometric approach to diabetic kidney disease can link structure to function and outcome.Eucalyptol ameliorates Snail1/β-catenin-dependent diabetic disjunction of renal tubular epithelial cells and tubulointerstitial fibrosis.A more tubulocentric view of diabetic kidney disease.Renal tubular ACE-mediated tubular injury is the major contributor to microalbuminuria in early diabetic nephropathy.Down-regulation of miR-23a inhibits high glucose-induced EMT and renal fibrogenesis by up-regulation of SnoN.Associations of urinary, glomerular, and tubular markers with the development of diabetic kidney disease in type 2 diabetes patients.CERA Attenuates Kidney Fibrogenesis in the db/db Mouse by Influencing the Renal Myofibroblast Generation.Ablation of FGFR2 in Fibroblasts Ameliorates Kidney Fibrosis after Ischemia/Reperfusion Injury in Mice.
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P2860
Can we target tubular damage to prevent renal function decline in diabetes?
description
2012 nî lūn-bûn
@nan
2012年の論文
@ja
2012年論文
@yue
2012年論文
@zh-hant
2012年論文
@zh-hk
2012年論文
@zh-mo
2012年論文
@zh-tw
2012年论文
@wuu
2012年论文
@zh
2012年论文
@zh-cn
name
Can we target tubular damage to prevent renal function decline in diabetes?
@ast
Can we target tubular damage to prevent renal function decline in diabetes?
@en
type
label
Can we target tubular damage to prevent renal function decline in diabetes?
@ast
Can we target tubular damage to prevent renal function decline in diabetes?
@en
prefLabel
Can we target tubular damage to prevent renal function decline in diabetes?
@ast
Can we target tubular damage to prevent renal function decline in diabetes?
@en
P2860
P1476
Can we target tubular damage to prevent renal function decline in diabetes?
@en
P2093
Joseph V Bonventre
P2860
P304
P356
10.1016/J.SEMNEPHROL.2012.07.008
P577
2012-09-01T00:00:00Z