Oxidative Stress as a Major Culprit in Kidney Disease in Diabetes
暂无分享,去创建一个
[1] M. Cooper,et al. Inhibition of NADPH Oxidase Prevents Advanced Glycation End Product–Mediated Damage in Diabetic Nephropathy Through a Protein Kinase C-α–Dependent Pathway , 2008, Diabetes.
[2] Anja Voigt,et al. Glucose restriction extends Caenorhabditis elegans life span by inducing mitochondrial respiration and increasing oxidative stress. , 2007, Cell metabolism.
[3] E. Bertini,et al. COQ2 nephropathy: a newly described inherited mitochondriopathy with primary renal involvement. , 2007, Journal of the American Society of Nephrology : JASN.
[4] F. DeRubertis,et al. Acceleration of diabetic renal injury in the superoxide dismutase knockout mouse: effects of tempol. , 2007, Metabolism: clinical and experimental.
[5] J. Ingelfinger,et al. Catalase overexpression attenuates angiotensinogen expression and apoptosis in diabetic mice. , 2007, Kidney international.
[6] D. Tripathi,et al. Intermittent fasting prevents the progression of type I diabetic nephropathy in rats and changes the expression of Sir2 and p53 , 2007, FEBS letters.
[7] J. Smeitink,et al. Superoxide production is inversely related to complex I activity in inherited complex I deficiency. , 2007, Biochimica et biophysica acta.
[8] M. Cooper,et al. Combination therapy with the advanced glycation end product cross-link breaker, alagebrium, and angiotensin converting enzyme inhibitors in diabetes: synergy or redundancy? , 2007, Endocrinology.
[9] Maristela L Onozato,et al. Double-Edged Action of SOD Mimetic in Diabetic Nephropathy , 2007, Journal of cardiovascular pharmacology.
[10] C. Forsblom,et al. A Functional Polymorphism in the Manganese Superoxide Dismutase Gene and Diabetic Nephropathy , 2007, Diabetes.
[11] J. Gross,et al. The Catalase –262C/T Promoter Polymorphism and Diabetic Complications in Caucasians with Type 2 Diabetes , 2007, Disease markers.
[12] C. Wilcox,et al. NADPH oxidases in the kidney. , 2006, Antioxidants & redox signaling.
[13] H. Kamijo,et al. Chronic Inhibition of Nitric Oxide Production Aggravates Diabetic Nephropathy in Otsuka Long-Evans Tokushima Fatty Rats , 2006, Nephron Physiology.
[14] A. Hipkiss. Does Chronic Glycolysis Accelerate Aging? Could This Explain How Dietary Restriction Works? , 2006, Annals of the New York Academy of Sciences.
[15] Min Zhu,et al. Calorie restriction mimetics: an emerging research field , 2006, Aging cell.
[16] M. Nangaku,et al. A severe diabetic nephropathy model with early development of nodule-like lesions induced by megsin overexpression in RAGE/iNOS transgenic mice. , 2006, Diabetes.
[17] B. Isermann,et al. Functional polymorphisms of UCP2 and UCP3 are associated with a reduced prevalence of diabetic neuropathy in patients with type 1 diabetes. , 2006, Diabetes care.
[18] M. Nangaku,et al. In a type 2 diabetic nephropathy rat model, the improvement of obesity by a low calorie diet reduces oxidative/carbonyl stress and prevents diabetic nephropathy. , 2005, Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association.
[19] H. Abboud,et al. Nox4 NAD(P)H Oxidase Mediates Hypertrophy and Fibronectin Expression in the Diabetic Kidney* , 2005, Journal of Biological Chemistry.
[20] J. Tavaré,et al. The human glomerular podocyte is a novel target for insulin action. , 2005, Diabetes.
[21] R. Atkins,et al. Kidney expression of glutathione peroxidase-1 is not protective against streptozotocin-induced diabetic nephropathy. , 2005, American journal of physiology. Renal physiology.
[22] V. Monnier,et al. Glycation of mitochondrial proteins from diabetic rat kidney is associated with excess superoxide formation. , 2005, American journal of physiology. Renal physiology.
[23] J. Arenas,et al. Renal pathology in children with mitochondrial diseases , 2005, Pediatric Nephrology.
[24] N. Komai,et al. NAD(P)H oxidase and uncoupled nitric oxide synthase are major sources of glomerular superoxide in rats with experimental diabetic nephropathy. , 2005, American journal of physiology. Renal physiology.
[25] Maristela L Onozato,et al. Effects of NADPH oxidase inhibitor in diabetic nephropathy. , 2005, Kidney international.
[26] Y. Sekino,et al. Osmotic Diuretics Induce Adenosine A1 Receptor Expression and Protect Renal Proximal Tubular Epithelial Cells against Cisplatin-mediated Apoptosis* , 2004, Journal of Biological Chemistry.
[27] S. Prabhakar. Role of nitric oxide in diabetic nephropathy. , 2004, Seminars in nephrology.
[28] F. Mohr,et al. Effect of a β2-Adrenoceptor Stimulation on Hyperglycemia-Induced Endothelial Dysfunction , 2004, Journal of Pharmacology and Experimental Therapeutics.
[29] M. Brand,et al. Prevention of mitochondrial oxidative damage as a therapeutic strategy in diabetes. , 2004, Diabetes.
[30] Simon Melov,et al. Endogenous mitochondrial oxidative stress: neurodegeneration, proteomic analysis, specific respiratory chain defects, and efficacious antioxidant therapy in superoxide dismutase 2 null mice , 2003, Journal of neurochemistry.
[31] F. Mohr,et al. Effect of a beta 2-adrenoceptor stimulation on hyperglycemia-induced endothelial dysfunction. , 2004, The Journal of pharmacology and experimental therapeutics.
[32] L. Denner,et al. Long-term renal effects of a neutralizing RAGE antibody in obese type 2 diabetic mice. , 2004, Diabetes.
[33] L. Scorrano,et al. Superoxide-mediated activation of uncoupling protein 2 causes pancreatic beta cell dysfunction. , 2003, The Journal of clinical investigation.
[34] E. Araki,et al. Reactive oxygen species from mitochondria induce cyclooxygenase-2 gene expression in human mesangial cells: potential role in diabetic nephropathy. , 2003, Diabetes.
[35] S. Matsumoto,et al. Confirmation of Superoxide Generation via Xanthine Oxidase in Streptozotocin-induced Diabetic Mice , 2003, Free radical research.
[36] V. D’Agati,et al. RAGE drives the development of glomerulosclerosis and implicates podocyte activation in the pathogenesis of diabetic nephropathy. , 2003, The American journal of pathology.
[37] A. Munnich,et al. Idebenone and reduced cardiac hypertrophy in Friedreich's ataxia , 2002, Heart.
[38] Maristela L Onozato,et al. Oxidative stress and nitric oxide synthase in rat diabetic nephropathy: effects of ACEI and ARB. , 2002, Kidney international.
[39] Zhiquan Zhang,et al. High Glucose Inhibits Glucose-6-phosphate Dehydrogenase via cAMP in Aortic Endothelial Cells* , 2000, The Journal of Biological Chemistry.
[40] M. Cooper,et al. Randomised controlled trial of dual blockade of renin-angiotensin system in patients with hypertension, microalbuminuria, and non-insulin dependent diabetes: the candesartan and lisinopril microalbuminuria (CALM) study , 2000, BMJ : British Medical Journal.
[41] G. Damante,et al. Defective intracellular antioxidant enzyme production in type 1 diabetic patients with nephropathy. , 2000, Diabetes.
[42] Y. Kaneda,et al. Normalizing mitochondrial superoxide production blocks three pathways of hyperglycaemic damage , 2000, Nature.
[43] Bruce H. R. Wolffenbuttel,et al. Effects of ramipril on cardiovascular and microvascular outcomes in people with diabetes mellitus: results of the HOPE study and MICRO-HOPE substudy , 2000, The Lancet.
[44] S. Yusuf,et al. Effects of ramipril on cardiovascular and microvascular outcomes in people with diabetes mellitus: results of the HOPE study and MICRO-HOPE substudy. Heart Outcomes Prevention Evaluation Study Investigators. , 2000 .
[45] Paul J Thornalley,et al. Formation of glyoxal, methylglyoxal and 3-deoxyglucosone in the glycation of proteins by glucose. , 1999, The Biochemical journal.
[46] S. Kim,et al. Role of Nitric Oxide in the Pathogenesis of Diabetic Nephropathy in Streptozotocin-Induced Diabetic Rats , 1999, The Korean journal of internal medicine.
[47] R. Holman,et al. Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). UK Prospective Diabetes Study (UKPDS) Group. , 1998 .
[48] Uk-Prospective-Diabetes-Study-Group. Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33) , 1998, The Lancet.
[49] M. Cooper,et al. Pathogenesis, prevention, and treatment of diabetic nephropathy , 1998, The Lancet.
[50] Paul J Thornalley. Glutathione-dependent detoxification of alpha-oxoaldehydes by the glyoxalase system: involvement in disease mechanisms and antiproliferative activity of glyoxalase I inhibitors. , 1998, Chemico-biological interactions.
[51] Paul J Thornalley,et al. Overexpression of glyoxalase-I in bovine endothelial cells inhibits intracellular advanced glycation endproduct formation and prevents hyperglycemia-induced increases in macromolecular endocytosis. , 1998, The Journal of clinical investigation.
[52] A. Munnich,et al. Aconitase and mitochondrial iron–sulphur protein deficiency in Friedreich ataxia , 1997, Nature Genetics.
[53] G. Jerums,et al. Relative contributions of advanced glycation and nitric oxide synthase inhibition to aminoguanidine-mediated renoprotection in diabetic rats , 1997, Diabetologia.
[54] M. Kobayashi,et al. Recombinant insulin-like growth factor I normalizes expression of renal glucose transporters in diabetic rats. , 1997, The American journal of physiology.
[55] G. King,et al. Prevention of glomerular dysfunction in diabetic rats by treatment with d-alpha-tocopherol. , 1997, Journal of the American Society of Nephrology : JASN.
[56] K. Federlin,et al. A benfotiamine-vitamin B combination in treatment of diabetic polyneuropathy. , 2009, Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association.
[57] P. Pandolfi,et al. Targeted disruption of the housekeeping gene encoding glucose 6‐phosphate dehydrogenase (G6PD): G6PD is dispensable for pentose synthesis but essential for defense against oxidative stress. , 1995, The EMBO journal.
[58] S. Freytag,et al. Overexpression of glucose transporters in rat mesangial cells cultured in a normal glucose milieu mimics the diabetic phenotype. , 1995, The Journal of clinical investigation.
[59] A. Schmidt,et al. Advanced glycation endproducts interacting with their endothelial receptor induce expression of vascular cell adhesion molecule-1 (VCAM-1) in cultured human endothelial cells and in mice. A potential mechanism for the accelerated vasculopathy of diabetes. , 1995, The Journal of clinical investigation.
[60] M. Cooper,et al. Role of Endothelium-Derived Nitric Oxide in the Pathogenesis of the Renal Hemodynamic Changes of Experimental Diabetes , 1994, Diabetes.
[61] R W Alexander,et al. Angiotensin II stimulates NADH and NADPH oxidase activity in cultured vascular smooth muscle cells. , 1994, Circulation research.
[62] J. Baynes,et al. Glycation, Glycoxidation, and Cross-Linking of Collagen by Glucose: Kinetics, Mechanisms, and Inhibition of Late Stages of the Maillard Reaction , 1994, Diabetes.
[63] K. O. Elliston,et al. Cloning and expression of a cell surface receptor for advanced glycosylation end products of proteins. , 1992, The Journal of biological chemistry.
[64] J. Turrens,et al. Generation of superoxide anion by the NADH dehydrogenase of bovine heart mitochondria. , 1980, The Biochemical journal.