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Review

Agents in development for the treatment of diabetic nephropathy

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Pages 279-294 | Published online: 22 Apr 2005

Bibliography

  • MAISONNEUVE P, AGODOA L, GELLERT R et al: Distribution of primary renal diseases leading to end-stage renal failure in the United States, Europe, and Australia/New Zealand: results from an international comparative study. Am. J. Kidney Dis. (2000) 35(1):157–165.
  • STRATTON IM, ADLER AT, NEIL HA et al.: Association of glycaemia with macrovascular and microvascular complications of type 2 diabetes (UKPDS 35): prospective observational study. Br. Med. 1 (2000) 321(728):405–412.
  • ADLER AT, STRATTON IM, NEIL HA et al.: Association of systolic blood pressure with macrovascular and microvascular complications of type 2 diabetes (UKPDS 36): prospective observationalstudy. BE Med. J. (2000) 321:412–419.
  • The Diabetes Control and Complications Trial Research Group: the effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. N Engl. J. Med. (1993) 329(14):977–986.
  • UK Prospective Diabetes Study (UKPDS) 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). Lancet (1998) 352:837–853.
  • COOPER ME: Interaction of metabolic and haemodynamic factors in mediating experimental diabetic nephropathy. Diabetologia (2001) 44(11):1957–1972.
  • ••A review of the pathogenetic mechanismsand interactions of the various pathways in the development of diabetic nephropathy.
  • LEWIS EJ, HUNSICKER LG, BAIN RP, ROHDE RD: The effect of angiotensin-converting-enzyme inhibition on diabetic nephropathy. The Collaborative Study Group. N Engl. J. Med. (1993) 329(20):1456–1462.
  • RAVID M, SAVIN H, JUTRIN I et al: Long-term stabilizing effect of angiotensin-converting enzyme inhibition on plasma creatinine and on proteinuria in normotensive type II diabetic patients. Ann. Intern. Med. (1993) 118(8):577–581.
  • SICA DA, BAKRIS GL: Type 2 diabetes: RENAAL and IDNT-the emergence of new treatment options. J. Clin. Hypertens. (Greenwich) (2002) 4(1):52–57.
  • KAGAMI S, BORDER WA, MILLER DE, NOBLE NA: Angiotensin II stimulates extracellular matrix protein synthesis through induction of transforming growth factor-13 expression in rat glomerular mesangial cells. J. Clin. Invest. (1994) 93(6):2431–2437.
  • ZIYADEH FN, HOFFMAN BB, HAN DC et al: Long-term prevention of renal insufficiency, excess matrix gene expression, and glomerular mesangial matrix expansion by treatment with monoclonal antitransforming growth factor-I3 antibody in db/db diabetic mice. Proc. Nati Acad. Sci. USA (2000) 97(14):8015–8020.
  • •This study provides evidence that treatment of TGF-13 antibody prevents the progression of diabetic nephropathy.
  • WEIGERT C, BRODBECK K, KLOPFER K, HARING HU, SCHLEICHER ED: Angiotensin II induces human TGF-131 promoter activation: similarity to hyperglycaemia. Diabetologia (2002) 45(6):890–898.
  • FUKAMI K, UEDA S, YAMAGISHI S et al.: AGEs activate mesangial TGF-13-Smad signaling via an angiotensin II type I receptor interaction. Kidney Int. (2004) 66(6):2137–2147.
  • FLYVBJERG A: Putative pathophysiological role of growth factors and cytokines in experimental diabetic kidney disease. Diabetologia (2000) 43(10):1205–1223.
  • ••An overview of the role of the growthhormone/insulin-like growth factor system and other cytokines in the pathogenesis of diabetic nephropathy.
  • MAKITA Z, RADOFF S, RAYFIELD EJ et al.: Advanced glycosylation end products in patients with diabetic nephropathy. N Engl. J. Med. (1991) 325(12):836–842.
  • VLASSARA H: Recent progress in advanced glycation end products and diabetic complications. Diabetes (1997) 46\(Suppl. 2):S19–S25.
  • FORBES JM, THALLAS-BONKE V, COOPER ME, THOMAS MC: Advanced glycation: how are we progressing to combat this web of sugar anomalies in diabetic nephropathy. Curr. Pharm. Des. (2004) 10(27):3361–3372.
  • •This paper demonstrates the role of AGEs and their receptors in diabetic nephropathy.
  • TSUCHIDA K, MAKITA Z, YAMAGISHI S et al.: Suppression of transforming growth factor 13 and vascular endothelial growth factor in diabetic nephropathy in rats by a novel advanced glycation end product inhibitor, OPB-9195. Diabetologia (1999) 42(5):579–588.
  • YAMAGISHI S, INAGAKI Y, OKAMOTO T et al.: Advanced glycation end products inhibit de novo protein synthesis and induce TGF-13 overexpression in proximal tubular cells. Kidney IrM (2003) 63(2):464–473.
  • FORBES JM, THALLAS V, THOMAS MC et al.: The breakdown of preexisting advanced glycation end products is associated with reduced renal fibrosis in experimental diabetes. FASEB J. (2003) 17(12):1762–1764.
  • FORBES JM, SOULIS T, THALLAS V et al.: Renoprotective effects of a novel inhibitor of advanced glycation. Diabetologia (2001) 44(1):108–114.
  • WAGMAN AS, NUSS JM: Current therapies and emerging targets for the treatment of diabetes. Curr. Pharm. Des. (2001) 7(6):417–450.
  • ELCHEBLY M, PAYETTE P, MICHALISZYN E et al.: Increased insulin sensitivity and obesity resistance in mice lacking the protein tyrosine phosphatase-1B gene. Science (1999) 283:1544–1548.
  • RING DB, JOHNSON KW, HENRIKSEN EJ et al.: Selective glycogen synthase kinase 3 inhibitors potentiate insulin activation of glucose transport and utilization in vitro and in vivo. Diabetes (2003) 52(3):588–595.
  • BEISSWENGER PJ, MAKITA Z, CURPHEY TJ et al: Formation of immunochemical advanced glycosylation end products precedes and correlates with early manifestations of renal and retinal disease in diabetes. Diabetes (1995) 44(7):824–829.
  • HORIE K, MIYATA T, MAEDA K et al: Immunohistochemical colocalization of glycoxidation products and lipid peroxidation products in diabetic renal glomerular lesions. Implication for glycoxidative stress in the pathogenesis of diabetic nephropathy..j Glib. Invest. (1997) 100(12):2995–3004.
  • SOULIS-LIPAROTA T, COOPER M, PAPAZOGLOU D, CLARKE B, JERUMS G: Retardation by aminoguanidine of development of albuminuria, mesangial expansion, and tissue fluorescence in streptozocin-induced diabetic rat. Diabetes (1991) 40(10):1328–1334.
  • ABDEL-RAHMAN E, BOLTON WK: Pimagedine: a novel therapy for diabetic nephropathy. Expert Opin. Investig. Drugs (2002) 11(4):565–574.
  • BROWN CD, ZHAO ZH, THOMAS LL, DEGROOF R, FRIEDMAN EA: Effects of erythropoietin and aminoguanidine on red blood cell deformability in diabetic azotemic and uremic patients. Am. I Kidney Dis. (2001) 38(6):1414–1420.
  • DEGENHARDT TP, ALDERSON NL, ARRINGTON DD et al: Pyridoxamine inhibits early renal disease and dyslipidemia in the streptozotocin-diabetic rat. Kidney Int. (2002) 61(3):939–950.
  • NAKAMURA S, MAKITA Z, ISHIKAWA S et al.: Progression of nephropathy in spontaneous diabetic rats is prevented by OPB-9195, a novel inhibitor of advanced glycation. Diabetes (1997) 46(5):895–899.
  • MIYATA T, UEDA Y, ASAHI K et al: Mechanism of the inhibitory effect of OPB-9195)-2- isopropylidenehydrazono-4-oxo-thiazolidin-5-yla cetanilidel on advanced glycation end product and advanced lipoxidation end product formation. J. Am. Soc. Nephrof (2000) 11(9):1719–1725.
  • FIGAROLA JL, SCOTT S, LOERA S et al: LR-90 a new advanced glycation endproduct inhibitor prevents progression of diabetic nephropathy in streptozotocin-diabetic rats. Diabetologia (2003) 46(8):1140–1152.
  • Effect of intensive blood-glucose control with metformin on complications in overweight patients with type 2 diabetes (UKPDS 34). UK Prospective Diabetes Study (UKPDS) Group. Lancet (1998) 352:854–865.
  • BEISSWENGER P, RUGGIEROLOPEZ D: Metformin inhibition of glycation processes. Diabetes Metab. (2003) 29(4 Pt 2):6595–103.
  • HAMMES HP, DU X, EDELSTEIN D et al: Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy. Nat. Med. (2003) 9(3):294–299.
  • BABAEI-JADIDI R, KARACHALIAS N, AHMED N, BATTAH S, THORNALLEY PJ: Prevention of incipient diabetic nephropathy by high-dose thiamine and benfotiamine. Diabetes (2003) 52(8):2110–2120.
  • NISHIKAWA T, EDELSTEIN D, DU XL et al: Normalizing mitochondrial superoxide production blocks three pathways of hyperglycaemic damage. Nature (2000) 404:787–790.
  • •This paper demonstrates the evidence for a critical role of mitochondrial oxidation in the activation various metabolic pathways, which may be involved in diabetic vascular complications.
  • VASAN S, ZHANG X, KAPURNIOTU A et al.: An agent cleaving glucose-derived protein crosslinks in vitro and in vivo. Nature (1996) 382:275–278.
  • VASAN S, FOILES P, FOUNDS H: Therapeutic potential of breakers of advanced glycation end product-protein crosslinks. Arch. Biochem. Biophys. (2003) 419(1):89–96.
  • WOLFFENBUTTEL BH, BOULANGER CM, CRIJNS FR et al: Breakers of advanced glycation end products restore large artery properties in experimental diabetes. Proc. Natl. Acad. Li. USA (1998) 95(8):4630–4634.
  • KASS DA, SHAPIRO EP, KAWAGUCHI M et al: Improved arterial compliance by a novel advanced glycation end-product crosslink breaker. Circulation (2001) 104(13):1464–1470.
  • OLDFIELD MD, BACH LA, FORBES JM et al: Advanced glycation end products cause epithelial-myofibroblast transdifferentiation via the receptor for advanced glycation end products (RAGE). Clin. Invest. (2001) 108(12):1853–1863.
  • ••This paper demonstrates for the first timethat AGEs promote tubular cells to adopt a fibroblast-like phenotype through the receptor RAGE and that this phenomenon may be involved in the pathogenesis of diabetic nephropathy.
  • WAUTIER MP, CHAPPEY 0, CORDA S et al.: Activation of NADPH oxidase by AGE links oxidant stress to altered gene expression via RAGE. Am. I Physiol. Endocrinol. Metab. (2001) 280(5):E685–E694.
  • KISLINGER T, FU C, HUBER B et al: N- (c) - (carb o xy m ethy lysine adducts of proteins are ligands for receptor for advanced glycation end products that activate cell signaling pathways and modulate gene expression. J. Biol. Chem. (1999) 274(44):31740–31749.
  • TANAKA N, YONEKURA H, YAMAGISHI S et al.: The receptor for advanced glycation end products is induced by the glycation products themselves and tumor necrosis factor-a through nuclear factor-KB, and by 1713-estradiol through Spl in human vascular endothelial cells..1. Biol. Chem. (2000) 275(33):25781–25790.
  • WENDT TM, TANJI N, GUO J et al: RAGE drives the development of glomerulosclerosis and implicates podocyte activation in the pathogenesis of diabetic nephropathy. Am. I Athol (2003) 162(4):1123–1137.
  • PARK L, RAMAN KG, LEE KJ et al: Suppression of accelerated diabetic atherosclerosis by the soluble receptor for advanced glycation endproducts. Nat. Med. (1998) 4(9):1025–1031.
  • •This paper demonstrates that sRAGE attenuates diabetes-induced atherosclerosis.
  • ZHENG F, CAI W, MITSUHASHI T et al.: Lysozyme enhances renal excretion of advanced glycation endproducts in vivo and suppresses adverse age-mediated cellular effects in vitro: a potential AGE sequestration therapy for diabetic nephropathy? Mol. Med. (2001) 7(11):737–47.
  • DUNLOP M: Aldose reductase and the roleof the polyol pathway in diabetic nephropathy. Kidney Int. Suppl. (2000) 77:S3–S12.
  • GABBAY KH: Hyperglycemia, polyol metabolism, and complications of diabetes mellitus. Ann. Rev Med (1975) 26:521–536.
  • PEDERSEN MM, CHRISTIANSEN JS, MOGENSEN CE: Reduction of glomerular hyperfiltration in normoalbuminuric IDDM patients by 6 mo of aldose reductase inhibition. Diabetes (1991) 40(5):527–531.
  • PASSARIELLO N, SEPE J, MARRAZZO G et al.: Effect of aldose reductase inhibitor (tolrestat) on urinary albumin excretion rate and glomerular filtration rate in IDDM subjects with nephropathy. Diabetes Care (1993) 16(5):789–795.
  • BEYER-MEARS A, MISTRY K, DIECKE FP, CRUZ E: Zopolrestat prevention of proteinuria, albuminuria and cataractogenesis in diabetes mellitus. Pharmacology (1996) 52(5):292–302.
  • MALAMAS MS, HOHMAN TC, MILLEN J: Novel spirosuccinimide aldose reductase inhibitors derived from isoquinoline-1,3-diones: 2-[(4-bromo-2-fluorophenyl)methyl]-6- fluorospiro risoquinoline-4 (1H)3'-pyrrolidinel-1,2',3,5'(2H)-tetrone and congeners. 1. J. Med. Chem. (1994) 37(13):2043–2058.
  • NAKAMURA N, YAMAZAKI K, SATOH A et al: Effects of eparlestat on plasma levels of advanced glycation end products in patients with type 2 diabetes. In vivo (2003) 17(2):177–180.
  • BROWNLEE M: Biochemistry and molecular cell biology of diabetic complications. Nature (2001) 414:813–820.
  • ••An excellent overview of the role of ROSfor the development of diabetic complications.
  • BAYNES JW, THORPE SR: Role of oxidative stress in diabetic complications: a new perspective on an old paradigm. Diabetes (1999) 48(1):1–9.
  • CAMERON NE, COTTER MA: Effects of antioxidants on nerve and vascular dysfunction in experimental diabetes. Diabetes Res. Clin. Pract. (1999) 45(2-3):137–146.
  • FORBES JM, COOPER ME, THALLAS V et al: Reduction of the accumulation of advanced glycation end products by ACE inhibition in experimental diabetic nephropathy. Diabetes (2002) 51(11):3274–3282.
  • COTTER MA, CAMERON NE: Effects of the NAD (P)H oxidase inhibitor, apocynin, on peripheral nerve perfusion and function in diabetic rats. Life Sci. (2003) 73(14):1813–1824.
  • SOULIS-LIPAROTA T, COOPER ME, DUNLOP M, JERUMS G: The relative roles of advanced glycation, oxidation and aldose reductase inhibition in the development of experimental diabetic nephropathy in the Sprague-Dawley rat. Diabetologia (1995) 38(4):387–394.
  • JANG YY, SONG JH, SHIN YK, HAN ES, LEE CS: Protective effect of boldine on oxidative mitochondrial damage in streptozotocin-induced diabetic rats. Pharmacol. Res. (2000) 42(4):361–371.
  • HEILIG CW, LIU Y, ENGLAND RL et al.: D-glucose stimulates mesangial cell GLUT1 expression and basal and IGF-I-sensitive glucose uptake in rat mesangial cells: implications for diabetic nephropathy. Diabetes (1997) 46(6):1030–1039.
  • INOKI K, HANEDA M, MAEDA S, KOYA D, KIKKAWA R: TGF-131 stimulates glucose uptake by enhancing GLUT1 expression in mesangial cells. Kidney Int. (1999) 55(5):1704–1712.
  • LOW BC, ROSS IK, GRIGOR MR: Angiotensin II stimulates glucose transport activity in cultured vascular smooth muscle cells. J. Biol. Chem. (1992) 267(29):20740–20745.
  • HENRY DN, BUSIK JV, BROSIUS FC III, HEILIG CW: Glucose transporters control gene expression of aldose reductase, PKCa, and GLUT1 in mesangial cells in vitro. Am. J. Physiol. (1999) 277(1 Pt 2):F97–104.
  • ADACHI T, YASUDA K, OKAMOTO Y et al: T-1095, a renal Nat-glucose transporter inhibitor, improves hyperglycemia in streptozotocin-induced diabetic rats. Metabolism (2000) 49(8):990–995.
  • KANWAR YS, ROSENZWEIG LJ, LINKER A, JAKUBOWSKI ML: Decreased de novo synthesis of glomerular proteoglycans in diabetes: biochemical and autoradiographic evidence. Proc. Natl. Acad Li. USA (1983) 80(8):2272–2275.
  • ROHRBACH DH, HASSELL JR, KLEINMAN HK, MARTIN GR: Alterations in the basement membrane (heparan sulfate) proteoglycan in diabetic mice. Diabetes (1982) 31(2):185–188.
  • ROHRBACH DH, WAGNER CW, STAR VU et al.: Reduced synthesis of basement membrane heparan sulfate proteoglycan in streptozotocin-induced diabetic mice. J. Biol. Chem. (1983) 258(19):11672–11677.
  • VAN DER PIJL JW, VAN DER WOUDE FJ, GEELHOED-DUIJVESTIJN PH et al.: Danaparoid sodium lowers proteinuria in diabetic nephropathy. I Am. Soc. Nephrol. (1997) 8(3):456–462.
  • SOLINI A, VERGNANI L, RICCI F, CREPALDI G: Glycosaminoglycans delay the progression of nephropathy in NIDDM. Diabetes Care (1997) 20(5):819–823.
  • POPLAWSKA A, SZELACHOWSKA M, TOPOLSKA J, WYSOCKA-SOLOWIE B, KINALSKA I: Effect of glycosaminoglycans on urinary albumin excretion in insulin-dependent diabetic patients with micro- or macroalbuminuria. Diabetes Res. Clin. Pract. (1997) 38(2):109–114.
  • DEDOV I, SHESTAKOVA M, VORONTZOV A, PALAZZINI E: A randomized, controlled study of sulodexide therapy for the treatment of diabetic nephropathy. Nephrol. Dial. Transplant. (1997) 12(11):2295–2300.
  • SZELACHOWSKA M, POPLAWSKA A, TOPOLSKA J et al: A pilot study of the effect of the glycosaminoglycan sulodexide on microalbuminuria in type I diabetic patients. Curr. Med. Res. Opin. (1997) 13(9):539–545.
  • •Phase II/III clinical trial to evaluate sulodexide for the treatment of diabetic nephropathy.
  • PARVING HH, LEHNERT H, BROCHNER-MORTENSEN J et al.: The effect of irbesartan on the development of diabetic nephropathy in patients with type 2 diabetes. N Engl. J. Med. (2001) 345(12):870–878.
  • ••An important clinical study of the effectsof ATI blockade in a group of subjects with Incipient diabetic nephropathy.
  • BRENNER BM, COOPER ME, DE ZEEUW D et al.: Effects of losartan on renal and cardiovascular outcomes in patients with type 2 diabetes and nephropathy. N Engl. I Med. (2001) 345(12):861–869.
  • ••An important clinical study of the effectsof ATI blockade on the progress of diabetic nephropathy.
  • LEWIS EJ, HUNSICKER LG, CLARKE WR et al.: Renoprotective effect of the angiotensin-receptor antagonist irbesartan in patients with nephropathy due to type 2 diabetes. N Engl. J. Med. (2001) 345(12):851–860.
  • ••An important clinical study of the effectsof ATI blockade in a group of subjects with Incipient diabetic nephropathy.
  • WOLF G, ZIYADEH FN, THAISS F et al.: Angiotensin II stimulates expression of the chemokine RANTES in rat glomerular endothelial cells. Role of the angiotensin type 2 receptor. J. Clin. Invest. (1997) 100(5):1047–1058.
  • CAO Z, KELLY DJ, COX A et al.: Angiotensin type 2 receptor is expressed in the adult rat kidney and promotes cellular proliferation and apoptosis. Kidney I'M (2000) 58(6):2437–2451.
  • SIRAGY HM, CAREY RIVI: The subtype 2 (AT2) angiotensin receptor mediates renal production of nitric oxide in conscious rats. Clin. Invest. (1997) 100(2):264–269.
  • SIRAGY HM, CAREY RM: The subtype-2 (AT2) angiotensin receptor regulates renal cyclic guanosine 3',5'-monophosphate and ATI receptor-mediated prostaglandin E2 production in conscious rats. J. Clin. Invest. (1996) 97(8):1978–1982.
  • CAO Z, BONNET F, CANDIDO R el al.: Angiotensin type 2 receptor antagonism confers renal protection in a rat model of progressive renal injury. I. Am. Soc. Nephrol. (2002) 13(7):1773–1787.
  • HARGROVE GM, DUFRESNE J, WHITESIDE C, MURUVE DA, WONG NC: Diabetes mellitus increases endothelin-1 gene transcription in rat kidney. Kidney Int. (2000) 58(4):1534–1545.
  • JANDELEIT-DAHM K, ALLEN TJ, YOUSSEF S, GILBERT RE, COOPER ME: Is there a role for endothelin antagonists in diabetic renal disease? Diabetes Obes. Metab. (2000) 2(1):15–24.
  • DING SS, QIU C, HESS P et al: Chronic endothelin receptor blockade prevents both early hyperfiltration and late overt diabetic nephropathy in the rat. J. Cardiovasc. Pharmacol. (2003) 42(1):48–54.
  • KOWALA MC, MURUGESAN N, TELLEW J et al.: Novel dual action ATI and ET-A receptor antagonists reduce blood pressure in experimental hypertension. I Pharmacol. Exp. Ther. (2004) 309(1):275–284.
  • ZERBE RU, VINICOR F, ROBERTSON GL: Plasma vasopressin in uncontrolled diabetes mellitus. Diabetes (1979) 28(5):503–508.
  • KAMOI K, ISHIBASHI M, YAMAJI T: Thirst and plasma levels of vasopressin, angiotensin II and atrial natriuretic peptide in patients with non-insulin-dependent diabetes mellitus. Diabetes Res. Clin. Pract. (1991) 11(3):195–202.
  • TALLROTH G, RYDING E, EKMAN R, AGARDH CD: The response of regulatory peptides to moderate hypoglycaemia of short duration in type 1 (insulin-dependent) diabetes mellitus and in normal man. Diabetes Res. (1992) 20(3):73–85.
  • NISHIKAWA T, OMURA M, IIZUKA T, SAITO I, YOSHIDA S: Short-term clinical trial of 1-(1-[4-(3-acetylaminopropoxy)-benzoyl]-4-piperidy1)-3, 4-dihydro-2(1H)-quinolinone in patients with diabetic nephropathy. Possible effectiveness of the specific vasopressin V1 receptor antagonist for reducing albuminuria in patients with non-insulin dependent diabetes mellitus. Arzneimittelforschung (1996) 46(9):875–878.
  • BURRELL LM, FARINA N, RISVANIS J et al: Inhibition of neutral endopeptidase, the degradative enzyme for natriuretic peptides, in rat kidney after oral SCH-42495. Clin. Sri. (1997) 93(1):43–50.
  • QUASCHNING T, GALLE J, WANNER C: Vasopeptidase inhibition: a new treatment approach for endothelial dysfunction. Kidney mt. (2003) 84:S54–S57.
  • SCHAFER S, LINZ W, VOLLERT H et al.: The vasopeptidase inhibitor AVE-7688 ameliorates type 2 diabetic nephropathy. Diabetologia (2004) 47(1):98–103.
  • DAVIS BJ, JOHNSTON CI, BURRELL LM et al.: Renoprotective effects of vasopeptidase inhibition in an experimental model of diabetic nephropathy. Diabetologia (2003) 46(7):961–971.
  • TIKKANEN I, TIKKANEN T, CAO Z et al.: Combined inhibition of neutral endopeptidase with angiotensin converting enzyme or endothelin converting enzyme in experimental diabetes. ./. Hypertens. (2002) 20(4):707–714.
  • KIRSCHENBAUM MA, CHAUDHARI A: Effect of experimental diabetes on glomerular filtration rate and glomerular prostanoid production in the rat. Miner. Electrolyte Metab. (1986) 12(5-6):352–355.
  • MOEL DI, SAFIRSTEIN RL, McEVOY RC, HSUEH W: Effect of aspirin on experimental diabetic nephropathy. J. Lab. Clin. Med. (1987) 110(3):300–307.
  • HOMMEL E, MATHIESEN E, ARNOLD-LARSEN S et al: Effects of indomethacin on kidney function in type 1 (insulin-dependent) diabetic patients with nephropathy. Diabetologia (1987) 30(2):78–81.
  • MAHADEVAN P, LARKINS RG, FRASER JR, DUNLOP ME: Effect of prostaglandin E2 and hyaluronan on mesangial cell proliferation. A potential contribution to glomerular hypercellularity in diabetes. Diabetes (1996) 45(1):44–50.
  • WOLF G, ZIYADEH FN: Molecular mechanisms of diabetic renal hypertrophy. Kidney mt. (1999) 56(2):393–405.
  • DEWITT DL, SMITH WL: Primary structure of prostaglandin G/H synthase from sheep vesicular gland determined from the complementary DNA sequence. Proc. Natl. Acad. Sci. USA (1988) 85(5):1412–1416.
  • KUJUBU DA, FLETCHER BS, VARNUM BC, LIM RW, HERS CHMAN HR: TIS10, a phorbol ester tumor promoter-inducible mRNA from Swiss 3T3 cells, encodes a novel prostaglandin synthase/cyclooxygenase homologue. .1 Biol. Chem. (1991) 266(20):12866–12872.
  • TETSUKA T, DAPHNA-IKEN D, MILLER BW et al.: Nitric oxide amplifies interleukin 1-induced cyclooxygenase-2 expression in rat mesangial cells. J. Clin. Invest. (1996) 97(9):2051–2056.
  • HARRIS RC, McKANNA JA, AKAI Y et al.: Cyclooxygenase-2 is associated with the macula densa of rat kidney and increases with salt restriction. .1 Clin. Invest. (1994) 94(6):2504–2510.
  • CHENG HF, WANG CJ, MOECKEL GW et al.: Cyclooxygenase-2 inhibitor blocks expression of mediators of renal injury in a model of diabetes and hypertension. Kidney Int. (2002) 62(3):929–939.
  • MAMDANI M, JUURLINK DN, LEE DS et al.: Cyclo-oxygenase-2 inhibitors versus non-selective non-steroidal anti-inflammatory drugs and congestive heart failure outcomes in elderly patients: a population-based cohort study. Lancet (2004) 363: 1751-1756.
  • OWADA A, SUDA S, HATA T: Effect of long-term administration of prostaglandin I(2) in incipient diabetic nephropathy. Nephron (2002) 92(4):788–796.
  • YAMASHITA T, SHIKATA K, MATSUDA M et al.: Beraprost sodium, prostacyclin analogue, attenuates glomerular hyperfiltration and glomerular macrophage infiltration by modulating ecNOS expression in diabetic rats. Diabetes Res. Clin. Pract. (2002) 57(3):149–161.
  • MATSUO Y, TAKAGAWA I, KOSHIDA H et al.: Antiproteinuric effect of a thromboxane receptor antagonist, S-1452, on rat diabetic nephropathy and murine lupus nephritis. Pharmacology (1995) 50(1):1–8.
  • OKUMURA M, IMANISHI M, OKAMURA M et al.: Role for thromboxane A2 from glomerular thrombi in nephropathy with type 2 diabetic rats. Life Sci. (2003) 72(24):2695–2705.
  • BORDER WA, NOBLE NA: Transforming growth factor 13 in tissue fibrosis. N Engl. Med. (1994) 331(19):1286–1292.
  • YAMAMOTO T, NAKAMURA T, NOBLE NA, RUOSLAHTI E, BORDER WA: Expression of transforming growth factor 13 is elevated in human and experimental diabetic nephropathy. Proc. Nati Acad. Sci. USA (1993) 90(5):1814–1818.
  • SHARMA K, JIN Y, GUO J, ZIYADEH FN: Neutralization of TGF-13 by anti-TGF-13 antibody attenuates kidney hypertrophy and the enhanced extracellular matrix gene expression in STZ-induced diabetic mice. Diabetes (1996) 45(4):522–530.
  • SHARMA K, ZIYADEH FN, ALZAHABI B et al.: Increased renal production of transforming growth factor-131 in patients with type II diabetes. Diabetes (1997) 46(5):854–859.
  • DAVIS BJ, FORBES JM, THOMAS MC et al.: Superior renoprotective effects of combination therapy with ACE and AGE inhibition in the diabetic spontaneously hypertensive rat. Diabetologia (2004) 47(1):89–97.
  • HILL C, FLYVBJERG A, RASCH R, BAK M, LOGAN A: Transforming growth factor-132 antibody attenuates fibrosis in the experimental diabetic rat kidney. Endocrinol (2001) 170(3):647–651.
  • CALLAHAN JF, BURGESS JL, FORNWALD JA et al.: Identification of novel inhibitors of the transforming growth factor In (TGF-131) type 1 receptor (ALK5). I Med. Chem. (2002) 45(5):999–1001.
  • KOGA K, YAMAGISHI S, TAKEUCHI M et al.: CS-886, a new angiotensin II type 1 receptor antagonist, ameliorates glomerular anionic site loss and prevents progression of diabetic nephropathy in Otsuka Long-Evans Tokushima fatty rats. Mol. Med. (2002) 8(10):591–599.
  • KELLY DJ, GILBERT RE, COX AJ et al.: Aminoguanidine ameliorates overexpression of prosclerotic growth factors and collagen deposition in experimental diabetic nephropathy. I Am. Soc. Nephrol. (2001) 12(10):2098–2107.
  • ROESTENBERG P, VAN NIEUWENHOVEN FA, WIETEN L et al.: Connective tissue growth factor is increased in plasma of type 1 diabetic patients with nephropathy. Diabetes Care (2004) 27(5):1164–1170.
  • TWIGG SM, CAO Z, SV MC et al.: Renal connective tissue growth factor induction in experimental diabetes is prevented by aminoguanidine. Endocrinology (2002) 143(12):4907–4915. 111.
  • RUPEREZ M, RUIZ-ORTEGA M, ESTEBAN V et al: Angiotensin II increases connective tissue growth factor in the kidney. Am. I Pathol (2003) 163(5):1937–1947.
  • TWIGG SM, COOPER ME: The time has come to target connective tissue growth factor in diabetic complications. Diabetologia (2004) 47(6):965–968.
  • FLYVBJERG A, KHATIR D, JENSEN UN et al: Long-term renal effects of a neutralizing connective tissue factor (CTG9-antibody in obese type 2 diabetic mice. J. Am. Soc. Nephrol (2004) 15:261A.
  • CANDIDO R, FORBES JM, THOMAS MC et al: A breaker of advanced glycation end products attenuates diabetes-induced myocardial structural changes. Circ. Res. (2003) 92(7):785–792.
  • TIKELLIS C, COOPER ME, TWIGG SM, BURNS WC, TOLCOS M: Connective tissue growth factor is up-regulated in the diabetic retina: amelioration by angiotensin-converting enzyme inhibition. Endocrinology (2004) 145(2):860–866.
  • YOKOI H, MUKOYAMA M, NAGAE T et al: Reduction in connective tissue growth factor by antisense treatment ameliorates renal tubulointerstitial fibrosis. J. Am. Soc. Nephrol (2004) 15(6):1430–1440.
  • GUHA M, XU Z, DEFALCO CY et al: Antisense oligonucleotides (AS0s) to connective tissue growth factor (CTGF) attenuates progression of diabetic nephropathy in mouse models of type 1 and type 2 diabetes. J. Am. Soc. Nephrol (2004) 15:29A.
  • AIELLO LP, AVERY RL, ARRIGG PG et al.: Vascular endothelial growth factor in ocular fluid of patients with diabetic retinopathy and other retinal disorders. N. Engl. J. Med. (1994) 331(22):1480–1487.
  • COOPER ME, VRANES D, YOUSSEF S et al.: Increased renal expression of vascular endothelial growth factor (VEGF) and its receptor VEGFR-2 in experimental diabetes. Diabetes (1999) 48(11):2229–2239.
  • DE VRIESE AS, TILTON RG, ELGER M et al.: Antibodies against vascular endothelial growth factor improve early renal dysfunction in experimental diabetes. Am. Soc. Nephrol (2001) 12(5):993–1000.
  • GILBERT RE, KELLY DJ, COX AJ et al: Angiotensin converting enzyme inhibition reduces retinal overexpression of vascular endothelial growth factor and hyperpermeability in experimental diabetes. Diabetologia (2000) 43(11):1360–1367.
  • MORAVSKI CJ, KELLY DJ, COOPER ME et al: Retinal neovascularization is prevented by blockade of the renin-angiotensin system. Hypertension (2000) 36(6):1099–1104.
  • SUNG, CHEN S, LAPING NJ et al: Albuminuria is ameliorated by an inhibition of VEGF receptors, 5U5416, in diabetic clb/clb mice but is unaffected in smad3-knockout mice rendered diabetic with streptozotocin. Am. Soc. Nephrol (2004) 15:720A.
  • FLYVBJERG A, DAGNAES-HANSEN F, DE VRIESE AS et al.: Amelioration of long-term renal changes in obese type 2 diabetic mice by a neutralizing vascular endothelial growth factor antibody. Diabetes (2002) 51(103090–3094.
  • HELDIN CH, WESTERMARK B: Platelet-derived growth factor: mechanism of action and possible in vivo function. Cell Rego]. (1990) 1(8):555–566.
  • FLOEGE J, ENG E, YOUNG BA et al.: Infusion of platelet-derived growth factor or basic fibroblast growth factor induces selective glomerular mesangial cell proliferation and matrix accumulation in rats. J. Clin. Invest. (1993) 92(6):2952–2962.
  • ISAKA Y, FUJIWARA Y, UEDA N et al: Glomerulosclerosis induced by in vivo transfection of transforming growth factor-0 or platelet-derived growth factor gene into the rat kidney. J. Clin. Invest. (1993) 92(6):2597–2601.
  • ROSS R: Platelet-derived growth factor. Lancet (1989) 1:1179–1182.
  • NAKAGAWA H, SASAHARA M, HANEDA M et al.: Immunohistochemical characterization of glomerular PDGF B-chain and PDGF 0-receptor expression in diabetic rats. Diabetes Res. Clin. Pratt (2000) 48(2):87–98.
  • GILBERT RE, KELLY DJ, McKAY T et al: PDGF signal transduction inhibition ameliorates experimental mesangial proliferative glomerulonephritis. Kidney Int. (2001) 59(4):1324–1332.
  • LASSILA M, JANDELEIT-DAHM K, SEAH KK et al.: Imatinib attenuates diabetic nephropathy in apolipoprotein E-knock out mice. I. Am. Soc. Nephrol (2005). In press.
  • GOLDMAN JM, MELO JV: Chronic myeloid leukemia-advances in biology and new approaches to treatment. N Engl. J. Med. (2003) 349(15):1451–1464.
  • FLYVBJERG A, LANDAU D, DOMENE H et al: The role of growth hormone, insulin-like growth factors (IGFs), and IGF-binding proteins in experimental diabetic kidney disease. Metabolism (1995) 44(10 Suppl. 4):67–71.
  • RAZ I, RUBINGER D, POPOVTZER M et al: Octreotide prevents the early increase in renal insulin-like growth factor binding protein 1 in streptozotocin diabetic rats. Diabetes (1998) 47(6):924–930.
  • BACH LA, COX AJ, MENDELSOHN FA et al: Focal induction of IGF binding proteins in proximal tubules of diabetic rat kidney. Diabetes (1992) 41(4):499–507.
  • BAK M, THOMSEN K, FLYVBJERG A: Effects of the somatostatin analogue octreotide on renal function in conscious diabetic rats. Nephrol Dial. Transplant (2001) 16(10):2002–2007.
  • AFARGAN M, JANSON ET, GELERMAN G et al: Novel long-acting somatostatin analog with endocrine selectivity: potent suppression of growth hormone but not of insulin. Endocrinology (2001) 142(1):477–486.
  • LANDAU D, SEGEV Y, AFARGAN M et al: A novel somatostatin analogue prevents early renal complications in the nonobese diabetic mouse. Kidney Int. (2001) 60(2):505–512.
  • FLYVBJERG A, BENNETT WE RASCH R, KOPCHICK JJ, SCARLETT JA: Inhibitory effect of a growth hormone receptor antagonist (G120K-PEG) on renal enlargement, glomerular hypertrophy, and urinary albumin excretion in experimental diabetes in mice. Diabetes (1999) 48(2):377–382.
  • PIETRZKOWSKI Z, WERNICKE D, PORCU P, JAMESON BA, BASERGA R: Inhibition of cellular proliferation by peptide analogues of insulin-like growth factor 1. Cancer Res. (1992) 52(23):6447–6451.
  • HAYLOR J, HICKLING H, EL ETER E et al: JB3, an IGF-I receptor antagonist, inhibits early renal growth in diabetic and uninephrectomized rats. Am. Soc. Nephrol (2000) 11(11):2027–2035.
  • XIA P, INOGUCHI T, KERN TS etal.: Characterization of the mechanism for the chronic activation of diacylglycerol-protein kinase C pathway in diabetes and hypergalactosemia. Diabetes (1994) 43(9):1122–1129.
  • KOYA D, JIROUSEK MR, LIN YW et al: Characterization of protein kinase C isoform activation on the gene expression of transforming growth factor-0, extracellular matrix components, and prostanoids in the glomeruli of diabetic rats. J. Clin. Invest. (1997) 100(1):115–126.
  • ISHII H, JIROUSEK MR, KOYA D et al: Amelioration of vascular dysfunctions in diabetic rats by an oral PKC 13 inhibitor. Science (1996) 272(5262):728–731.
  • MENNE J, PARK JK, BOEHNE M et al.: Diminished loss of proteoglycans and lack of albuminuria in protein kinase C-a-deficient diabetic mice. Diabetes (2004) 53(8):2101–2109.
  • THALLAS-BONKE V, LINDSCHAU C, RIZKALLA B et al.: Attenuation of extracellular matrix accumulation in diabetic nephropathy by the advanced glycation end product cross-link breaker ALT-711 via a protein kinase C-a-dependent pathway. Diabetes (2004) 53(1 0:2921–2930.
  • BARNES PJ, KARIN M: Nuclear factor-KB: a pivotal transcription factor in chronic inflammatory diseases. N Engl. J. Med. (1997) 336(15):1066–1071.
  • PIEPER GM, RIAZ-UL H: Activation of nuclear factor-KB in cultured endothelial cells by increased glucose concentration: prevention by calphostin C. I Cardiovasc. Pharmacol (1997) 30(4):528–532.
  • YAN SD, SCHMIDT AM, ANDERSON GM et al: Enhanced cellular oxidant stress by the interaction of advanced glycation end products with their receptors/ binding proteins. J. Biol. Chem. (1994) 269(13):9889–9897.
  • TAMADA S, NAKATANI T, ASAI T et al: Inhibition of nuclear factor-KB activation by pyrrolidine dithiocarbamate prevents chronic FK506 nephropathy. Kidney Int. (2003) 63(1):306–314.
  • LEE FT, CAO Z, LONG DM et al: Interactions between angiotensin II and NF-KB-dependent pathways in modulating macrophage infiltration in experimental diabetic nephropathy. J. Am. Soc. Nephrol (2004) 15(8):2139–2151.
  • TOMLINSON DR: Mitogen-activated protein kinases as glucose transducers for diabetic complications. Diabetologia (1999) 42(10:1271–1281.
  • AWAZU M, ISHIKURA K, HIDA M, HOSHIYA M: Mechanisms of mitogen-activated protein kinase activation in experimental diabetes. J. Am. Soc. Nephrol (1999) 10(4):738–745.
  • FUJITA H, OMORI S, ISHIKURA K, HIDA M, AWAZU M: ERK and p38 mediate high-glucose-induced hypertrophy and TGF-I3 expression in renal tubular cells. Am.. Physiol Renal Physiol (2004) 286(1):F120–F126.
  • LI JH, HUANG XR, ZHU HJ et al: Advanced glycation end products activate Smad signaling via TGF-13-dependent and independent mechanisms: implications for diabetic renal and vascular disease. FASEBI. (2004) 18(1):176–178.
  • KANG MJ, WU X, LY H, THAI K, SCHOLEY JW: Effect of glucose on stress-activated protein kinase activity in mesangial cells and diabetic glomeruli. Kidney mt. (1999) 55(6):2203–2214.
  • HANEDA M, ARAKI S, TOGAWA M et al.: Mitogen-activated protein kinase cascade is activated in glomeruli of diabetic rats and glomerular mesangial cells cultured under high glucose conditions. Diabetes (1997) 46(5):847–853.
  • ZHANG SL, TANG SS, CHEN X et al: High levels of glucose stimulate angiotensinogen gene expression via the P38 mitogen-activated protein kinase pathway in rat kidney proximal tubular cells. Endocrinology (2000) 141(12):4637–4646.
  • STAMBE C, ATKINS RC, TESCH GH et al.: Blockade of p38a MAPK ameliorates acute inflammatory renal injury in rat anti-GBM glomerulonephritis. J. Am. Soc. Nephrol (2003) 14(2):338–351.
  • American Diabetes Association: Diabetic Nephropathy. Diabetes Care (2002) 25:S85–S89.
  • http://www.alteon.com/pimagl.htm Website for the ACTION clinical trials.
  • http://www.alteon.com/crossl.htm Website for the DIAMOND trial.
  • http://www.ttpharma.com Transtech Pharma.
  • http://www.keryx.com/ Phase II/III clinical trial to evaluate sulodexide for the treatment of diabetic nephropathy.
  • http://www.vioxx.com Website for worldwide withdrawal of the COX-2 inhibitor rofecoxib.
  • http://www.fibrogen.com/trials/ Clinical trials for diabetic nephropathy and idiopathic pulmonary fibrosis.
  • hap://www.clinicaltrials.govict/show/ NCT00044148 Clinical trial of the effect of LY333531 on protein in the urine of patients with Type 2 diabetes.

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