Podocyte-specific Nox4 deletion affords renoprotection in a mouse model of diabetic nephropathy

[1]  H. Abboud,et al.  Targeting NADPH oxidase with a novel dual Nox1/Nox4 inhibitor attenuates renal pathology in type 1 diabetes. , 2015, American journal of physiology. Renal physiology.

[2]  Merlin C. Thomas,et al.  AT2R Agonist, Compound 21, Is Reno-Protective Against Type 1 Diabetic Nephropathy , 2015, Hypertension.

[3]  H. Abboud,et al.  NADPH Oxidase 4 Induces Cardiac Fibrosis and Hypertrophy Through Activating Akt/mTOR and NF&kgr;B Signaling Pathways , 2015, Circulation.

[4]  H. Schmidt,et al.  Nox‐4 deletion reduces oxidative stress and injury by PKC‐α‐associated mechanisms in diabetic nephropathy , 2014, Physiological reports.

[5]  R. Touyz,et al.  Genetic targeting or pharmacologic inhibition of NADPH oxidase nox4 provides renoprotection in long-term diabetic nephropathy. , 2014, Journal of the American Society of Nephrology : JASN.

[6]  R. Touyz,et al.  Nephropathy and elevated BP in mice with podocyte-specific NADPH oxidase 5 expression. , 2014, Journal of the American Society of Nephrology : JASN.

[7]  Merlin C. Thomas,et al.  Genetic deletion of cell division autoantigen 1 retards diabetes-associated renal injury. , 2013, Journal of the American Society of Nephrology : JASN.

[8]  H. Haller,et al.  Dual Inhibition of Classical Protein Kinase C-α and Protein Kinase C-β Isoforms Protects Against Experimental Murine Diabetic Nephropathy , 2013, Diabetes.

[9]  Jin Sook Kim,et al.  Renal Podocyte Injury in a Rat Model of Type 2 Diabetes Is Prevented by Metformin , 2012, Experimental diabetes research.

[10]  Bancha Satirapoj,et al.  Nephropathy in Diabetes , 2023, Experimental and Clinical Endocrinology & Diabetes.

[11]  M. Schiffer,et al.  PKCα Mediates β-Arrestin2-dependent Nephrin Endocytosis in Hyperglycemia* , 2011, The Journal of Biological Chemistry.

[12]  M. Ghazizadeh,et al.  Validation of Glomerular Basement Membrane Thickness Changes with Aging in Minimal Change Disease , 2011, Pathobiology.

[13]  P. Pinton,et al.  Redox control of protein kinase C: cell- and disease-specific aspects. , 2010, Antioxidants & redox signaling.

[14]  Jai Radhakrishnan,et al.  Pathologic classification of diabetic nephropathy. , 2010, Journal of the American Society of Nephrology : JASN.

[15]  N. Calcutt,et al.  Therapies for hyperglycaemia-induced diabetic complications: from animal models to clinical trials , 2009, Nature Reviews Drug Discovery.

[16]  H. Abboud,et al.  Mechanisms of Podocyte Injury in Diabetes , 2009, Diabetes.

[17]  R. Osterby,et al.  Improvement of blood glucose control in IDDM patients retards the progression of morphological changes in early diabetic nephropathy , 1994, Diabetologia.

[18]  Merlin C. Thomas,et al.  The endothelin receptor antagonist avosentan ameliorates nephropathy and atherosclerosis in diabetic apolipoprotein E knockout mice , 2009, Diabetologia.

[19]  G. Wolf,et al.  Pathogenesis of the podocytopathy and proteinuria in diabetic glomerulopathy. , 2008, Current diabetes reviews.

[20]  H. Kaneto,et al.  Involvement of oxidative stress in the pathogenesis of diabetes. , 2006, Antioxidants & redox signaling.

[21]  F. Ziyadeh,et al.  Blockade of vascular endothelial growth factor signaling ameliorates diabetic albuminuria in mice. , 2006, Journal of the American Society of Nephrology : JASN.

[22]  H. Haller,et al.  Nephrin loss in experimental diabetic nephropathy is prevented by deletion of protein kinase C alpha signaling in-vivo. , 2006, Kidney international.

[23]  C. Wilcox,et al.  NADPH oxidases in the kidney. , 2006, Antioxidants & redox signaling.

[24]  Jaakko Patrakka,et al.  Hereditary proteinuria syndromes and mechanisms of proteinuria. , 2006, The New England journal of medicine.

[25]  R. Atkins,et al.  Monocyte chemoattractant protein-1 promotes the development of diabetic renal injury in streptozotocin-treated mice. , 2006, Kidney international.

[26]  M. Schiffer,et al.  Glucose-induced reactive oxygen species cause apoptosis of podocytes and podocyte depletion at the onset of diabetic nephropathy. , 2006, Diabetes.

[27]  H. Abboud,et al.  Nox4 NAD(P)H Oxidase Mediates Hypertrophy and Fibronectin Expression in the Diabetic Kidney* , 2005, Journal of Biological Chemistry.

[28]  Colin Mathers,et al.  The burden of mortality attributable to diabetes: realistic estimates for the year 2000. , 2005, Diabetes care.

[29]  G. Wolf,et al.  From the periphery of the glomerular capillary wall toward the center of disease: podocyte injury comes of age in diabetic nephropathy. , 2005, Diabetes.

[30]  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.

[31]  Maristela L Onozato,et al.  Effects of NADPH oxidase inhibitor in diabetic nephropathy. , 2005, Kidney international.

[32]  F. Lai,et al.  Isolate diffuse thickening of glomerular capillary basement membrane: a renal lesion in prediabetes? , 2004, Modern Pathology.

[33]  Merlin C. Thomas,et al.  Accelerated nephropathy in diabetic apolipoprotein e-knockout mouse: role of advanced glycation end products. , 2004, Journal of the American Society of Nephrology : JASN.

[34]  R. Østerby,et al.  Glomerular epithelial foot processes and filtration slits in IDDM patients , 1995, Diabetologia.

[35]  G. Camussi,et al.  Nephrin expression is reduced in human diabetic nephropathy: evidence for a distinct role for glycated albumin and angiotensin II. , 2003, Diabetes.

[36]  M. Cooper,et al.  Role of nephrin in renal disease including diabetic nephropathy. , 2002, Seminars in nephrology.

[37]  B. Kasinath,et al.  Angiotensin II induces apoptosis in rat glomerular epithelial cells. , 2002, American journal of physiology. Renal physiology.

[38]  E. Bottinger,et al.  Apoptosis in podocytes induced by TGF-β and Smad7 , 2001 .

[39]  M. Cooper,et al.  Podocyte foot process broadening in experimental diabetic nephropathy: amelioration with renin-angiotensin blockade , 2001, Diabetologia.

[40]  A. Jesaitis,et al.  Phosphatidic Acid and Diacylglycerol Directly Activate NADPH Oxidase by Interacting with Enzyme Components* , 2001, The Journal of Biological Chemistry.

[41]  J. Morrow,et al.  F(2)-isoprostanes mediate high glucose-induced TGF-beta synthesis and glomerular proteinuria in experimental type I diabetes. , 2000, Kidney international.

[42]  M. Cooper,et al.  Increased renal expression of vascular endothelial growth factor (VEGF) and its receptor VEGFR-2 in experimental diabetes. , 1999, Diabetes.

[43]  J. Hodgin,et al.  A noninvasive computerized tail-cuff system for measuring blood pressure in mice. , 1995, Hypertension.

[44]  R. Butkowski,et al.  Differential expression of basement membrane collagen chains in diabetic nephropathy. , 1991, The American journal of pathology.

[45]  A. Michael,et al.  Polyantigenic Expansion of Basement Membrane Constituents in Diabetic Nephropathy , 1983, Diabetes.

[46]  B. Brenner,et al.  Molecular basis of proteinuria of glomerular origin. , 1978, The New England journal of medicine.