Josephine M Forbes

Summary

Country: Australia

Publications

  1. pmc Advanced glycation end products are direct modulators of β-cell function
    Melinda T Coughlan
    Division of Diabetes Complications, Diabetes and Metabolism Division, Baker IDI Heart and Diabetes Institute, Melbourne, Australia
    Diabetes 60:2523-32. 2011
  2. doi request reprint Glycation in diabetic nephropathy
    Josephine M Forbes
    Division of Diabetes Complications, Glycation and Diabetes, Baker IDI Heart and Diabetes Institute, St Kilda Rd Central, P O Box 6492, Melbourne, Vic, 8008, Australia
    Amino Acids 42:1185-92. 2012
  3. doi request reprint Receptor for advanced glycation end-products (RAGE) provides a link between genetic susceptibility and environmental factors in type 1 diabetes
    J M Forbes
    Diabetes Complications Division, Baker IDI Heart and Diabetes Institute, St Kilda Rd Central, P O Box 6492, Melbourne, VIC 8008, Australia
    Diabetologia 54:1032-42. 2011
  4. pmc The physiological deadlock between AMPK and gluconeogenesis: SOGA, a novel protein, may provide the key
    Josephine M Forbes
    Diabetes Division, Baker IDI Heart and Diabetes Institute, and the Department of Immunology, Monash University, Melbourne, Australia
    Am J Pathol 177:1600-2. 2010
  5. doi request reprint Disparate effects on renal and oxidative parameters following RAGE deletion, AGE accumulation inhibition, or dietary AGE control in experimental diabetic nephropathy
    Adeline L Y Tan
    Juvenile Diabetes Research Foundation Einstein Centre for Diabetic Complications, Baker International Diabetes Institute Heart and Diabetes Research Institute, Melbourne, Victoria, Australia
    Am J Physiol Renal Physiol 298:F763-70. 2010
  6. ncbi request reprint Combination therapy with the advanced glycation end product cross-link breaker, alagebrium, and angiotensin converting enzyme inhibitors in diabetes: synergy or redundancy?
    Melinda T Coughlan
    Albert Einstein Juvenile Diabetes Research Foundation Centre for Diabetes Complications, Wynn Domain, Baker Medical Research Institute, P O Box 6492, St Kilda Road Central, Melbourne, Victoria 8008, Australia
    Endocrinology 148:886-95. 2007
  7. doi request reprint The pleiotropic actions of rosuvastatin confer renal benefits in the diabetic Apo-E knockout mouse
    Sara Giunti
    Baker IDI Heart and Diabetes Institute, Monash University, Melbourne, Australia
    Am J Physiol Renal Physiol 299:F528-35. 2010
  8. ncbi request reprint Accelerated nephropathy in diabetic apolipoprotein e-knockout mouse: role of advanced glycation end products
    Markus Lassila
    Danielle Alberti Memorial Centre for Diabetes Complications, Vascular Division, Wynn Domain, Baker Heart Research Institute, Melbourne, Victoria, Australia
    J Am Soc Nephrol 15:2125-38. 2004
  9. doi request reprint Preservation of kidney function with combined inhibition of NADPH oxidase and angiotensin-converting enzyme in diabetic nephropathy
    Vicki Thallas-Bonke
    JDRF Einstein Centre for Diabetes Complications, Diabetes Complications Division, Baker IDI Heart and Diabetes Institute, Melbourne, Vic, Australia
    Am J Nephrol 32:73-82. 2010
  10. ncbi request reprint Inhibition of NADPH oxidase prevents advanced glycation end product-mediated damage in diabetic nephropathy through a protein kinase C-alpha-dependent pathway
    Vicki Thallas-Bonke
    JDRF Albert Einstein Centre for Diabetes Complications, Diabetes and Metabolism Division, Baker Medical Research Institute, P O Box 6492, St Kilda Rd, Central, Melbourne, Victoria, Australia
    Diabetes 57:460-9. 2008

Collaborators

Detail Information

Publications59

  1. pmc Advanced glycation end products are direct modulators of β-cell function
    Melinda T Coughlan
    Division of Diabetes Complications, Diabetes and Metabolism Division, Baker IDI Heart and Diabetes Institute, Melbourne, Australia
    Diabetes 60:2523-32. 2011
    ..Excess accumulation of advanced glycation end products (AGEs) contributes to aging and chronic diseases. We aimed to obtain evidence that exposure to AGEs plays a role in the development of type 1 diabetes (T1D)...
  2. doi request reprint Glycation in diabetic nephropathy
    Josephine M Forbes
    Division of Diabetes Complications, Glycation and Diabetes, Baker IDI Heart and Diabetes Institute, St Kilda Rd Central, P O Box 6492, Melbourne, Vic, 8008, Australia
    Amino Acids 42:1185-92. 2012
    ..Therefore, it has become apparent that decreasing the accumulation of AGEs or interrupting their downstream effects on the kidney, are desirable therapeutic targets for the treatment of diabetic renal disease...
  3. doi request reprint Receptor for advanced glycation end-products (RAGE) provides a link between genetic susceptibility and environmental factors in type 1 diabetes
    J M Forbes
    Diabetes Complications Division, Baker IDI Heart and Diabetes Institute, St Kilda Rd Central, P O Box 6492, Melbourne, VIC 8008, Australia
    Diabetologia 54:1032-42. 2011
    ..This group of studies examines human genetic susceptibility conferred by the receptor for advanced glycation end-products (RAGE) in type 1 diabetes and investigates how this may interact with a western environment...
  4. pmc The physiological deadlock between AMPK and gluconeogenesis: SOGA, a novel protein, may provide the key
    Josephine M Forbes
    Diabetes Division, Baker IDI Heart and Diabetes Institute, and the Department of Immunology, Monash University, Melbourne, Australia
    Am J Pathol 177:1600-2. 2010
    ..This Commentary discusses how suppressor of glucose by autophagy (SOGA) contributes to adiponectin-mediated insulin-dependent inhibition of autophagy during the activation of adenosine monophosphate kinase (AMPK)...
  5. doi request reprint Disparate effects on renal and oxidative parameters following RAGE deletion, AGE accumulation inhibition, or dietary AGE control in experimental diabetic nephropathy
    Adeline L Y Tan
    Juvenile Diabetes Research Foundation Einstein Centre for Diabetic Complications, Baker International Diabetes Institute Heart and Diabetes Research Institute, Melbourne, Victoria, Australia
    Am J Physiol Renal Physiol 298:F763-70. 2010
    ..In the present study, diverse approaches to block the AGE-RAGE axis had disparate effects on DN, which has potential clinical implications for the way this axis should be targeted in humans...
  6. ncbi request reprint Combination therapy with the advanced glycation end product cross-link breaker, alagebrium, and angiotensin converting enzyme inhibitors in diabetes: synergy or redundancy?
    Melinda T Coughlan
    Albert Einstein Juvenile Diabetes Research Foundation Centre for Diabetes Complications, Wynn Domain, Baker Medical Research Institute, P O Box 6492, St Kilda Road Central, Melbourne, Victoria 8008, Australia
    Endocrinology 148:886-95. 2007
    ....
  7. doi request reprint The pleiotropic actions of rosuvastatin confer renal benefits in the diabetic Apo-E knockout mouse
    Sara Giunti
    Baker IDI Heart and Diabetes Institute, Monash University, Melbourne, Australia
    Am J Physiol Renal Physiol 299:F528-35. 2010
    ..The combination treatment is not superior to monotherapies...
  8. ncbi request reprint Accelerated nephropathy in diabetic apolipoprotein e-knockout mouse: role of advanced glycation end products
    Markus Lassila
    Danielle Alberti Memorial Centre for Diabetes Complications, Vascular Division, Wynn Domain, Baker Heart Research Institute, Melbourne, Victoria, Australia
    J Am Soc Nephrol 15:2125-38. 2004
    ..The accelerated renal injury that was observed in diabetic apo E-KO mice was attenuated by approaches that inhibit renal AGE accumulation...
  9. doi request reprint Preservation of kidney function with combined inhibition of NADPH oxidase and angiotensin-converting enzyme in diabetic nephropathy
    Vicki Thallas-Bonke
    JDRF Einstein Centre for Diabetes Complications, Diabetes Complications Division, Baker IDI Heart and Diabetes Institute, Melbourne, Vic, Australia
    Am J Nephrol 32:73-82. 2010
    ..The aim of this study was to determine if there were added renoprotective benefits seen by combining ACEi with blockade of NADPH oxidase...
  10. ncbi request reprint Inhibition of NADPH oxidase prevents advanced glycation end product-mediated damage in diabetic nephropathy through a protein kinase C-alpha-dependent pathway
    Vicki Thallas-Bonke
    JDRF Albert Einstein Centre for Diabetes Complications, Diabetes and Metabolism Division, Baker Medical Research Institute, P O Box 6492, St Kilda Rd, Central, Melbourne, Victoria, Australia
    Diabetes 57:460-9. 2008
    ..Since NADPH oxidase activation is closely linked to other putative pathways, its interaction with changes in protein kinase C (PKC) and increased advanced glycation was examined...
  11. pmc Receptor for advanced glycation end products (RAGE) deficiency attenuates the development of atherosclerosis in diabetes
    Aino Soro-Paavonen
    Albert Einstein Juvenile Diabetes Research Foundation Centre for Diabetes Complications, Diabetes Metabolism Division, Baker Heart Research Institute, Melbourne, Australia
    Diabetes 57:2461-9. 2008
    ..This study examines the effects of deletion of RAGE on the development of atherosclerosis in the diabetic apoE(-/-) model of accelerated atherosclerosis...
  12. ncbi request reprint Modulation of soluble receptor for advanced glycation end products by angiotensin-converting enzyme-1 inhibition in diabetic nephropathy
    Josephine M Forbes
    Address correspondence to Dr Josephine Forbes, Danielle Alberti Memorial Centre for Diabetes Complications, Baker Heart Research Institute, P O Box 6492, St Kilda Road, Melbourne, Victoria, 8008, Australia
    J Am Soc Nephrol 16:2363-72. 2005
    ..It is postulated that ACE inhibition reduces the accumulation of AGE in diabetes partly by increasing the production and secretion of sRAGE into plasma...
  13. pmc Advanced glycation urinary protein-bound biomarkers and severity of diabetic nephropathy in man
    Melinda T Coughlan
    Glycation and Diabetes Complications, Baker IDI Heart and Diabetes Institute, St Kilda Rd Central, Melbourne, VIC 8008, Australia
    Am J Nephrol 34:347-55. 2011
    ..The aim of this study was to ascertain if the urinary excretion of proteins modified by advanced glycation can be used as biomarkers for albuminuria in individuals with type 1 or type 2 diabetes...
  14. doi request reprint Ubiquinone (coenzyme Q10) prevents renal mitochondrial dysfunction in an experimental model of type 2 diabetes
    Karly C Sourris
    Glycation and Diabetes Complications, Baker IDI Heart Research Institute, Melbourne, VIC 3004, Australia
    Free Radic Biol Med 52:716-23. 2012
    ..Therefore CoQ10 supplementation may be renoprotective in type 2 diabetes, via preservation of mitochondrial function...
  15. pmc Cardiac inflammation associated with a Western diet is mediated via activation of RAGE by AGEs
    Christos Tikellis
    Baker Medical Research Institute, Melbourne, Victoria 8008, Australia
    Am J Physiol Endocrinol Metab 295:E323-30. 2008
    ..These data point to the potential utility of AGE-reducing strategies in the prevention and management of cardiac disease...
  16. pmc RAGE-induced cytosolic ROS promote mitochondrial superoxide generation in diabetes
    Melinda T Coughlan
    Juvenile Diabetes Research Foundation Einstein Centre for Diabetes Complications, Division of Diabetes Complications, Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia
    J Am Soc Nephrol 20:742-52. 2009
    ....
  17. doi request reprint Targeted reduction of advanced glycation improves renal function in obesity
    Brooke E Harcourt
    Baker IDI Heart and Diabetes Research Institute, Melbourne, Victoria, Australia
    Kidney Int 80:190-8. 2011
    ..Thus, targeted reduction of the advanced glycation pathway improved renal function in obesity...
  18. ncbi request reprint Connective tissue growth factor plays an important role in advanced glycation end product-induced tubular epithelial-to-mesenchymal transition: implications for diabetic renal disease
    Wendy C Burns
    Danielle Alberti Memorial Centre for Diabetes Complications, Baker Heart Research Institute, PO Box 6492, St Kilda Road Central, Melbourne, Victoria, 8008, Australia
    J Am Soc Nephrol 17:2484-94. 2006
    ..This interaction is likely to play an important role in progressive diabetic nephropathy and strengthens the rationale to consider CTGF as a potential target for the treatment of diabetic nephropathy...
  19. doi request reprint Deficiency in mitochondrial complex I activity due to Ndufs6 gene trap insertion induces renal disease
    Josephine M Forbes
    Glycation, Nutrition and Metabolism Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, Australia
    Antioxid Redox Signal 19:331-43. 2013
    ..To determine whether an abnormality in mitochondrial complex I per se is associated with development of renal disease, mice with a knockdown of the complex I gene, Ndufs6 were studied...
  20. ncbi request reprint The breakdown of preexisting advanced glycation end products is associated with reduced renal fibrosis in experimental diabetes
    Josephine M Forbes
    Division of Diabetic Complications, Baker Medical Research Institute, Melbourne, Australia
    FASEB J 17:1762-4. 2003
    ....
  21. doi request reprint Oxidative stress as a major culprit in kidney disease in diabetes
    Josephine M Forbes
    Juvenile Diabetes Research Foundation Albert Einstein Centre for Diabetes Complications, Division of Diabetes and Metabolism, Baker Heart Research Institute, Melbourne, Australia
    Diabetes 57:1446-54. 2008
    ....
  22. doi request reprint Temporal increases in urinary carboxymethyllysine correlate with albuminuria development in diabetes
    Melinda T Coughlan
    Glycation and Diabetes Complications Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, Vic, Australia
    Am J Nephrol 34:9-17. 2011
    ..In this study, we investigated the temporal accumulation of the AGE carboxymethyllysine (CML) at various sites in a model of experimental diabetic nephropathy...
  23. doi request reprint Targeting the AGE-RAGE axis improves renal function in the context of a healthy diet low in advanced glycation end-product content
    Vicki Thallas-Bonke
    Diabetes Complications Division, Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia
    Nephrology (Carlton) 18:47-56. 2013
    ..The aim of this study was to evaluate if targeting of the AGE-RAGE axis was still effective in the context of a diet low in AGE content, which is more comparable to diets consumed by individuals with type 1 diabetes...
  24. ncbi request reprint Renal microvascular injury in diabetes: RAGE and redox signaling
    Melinda T Coughlan
    Albert Einstein Centre for Diabetes Complications, Wynn Domain, Baker Heart Research Institute, Melbourne, Victoria, Australia
    Antioxid Redox Signal 9:331-42. 2007
    ..This review focuses on how ROS play a deleterious role in the diabetic kidney and how they are involved in crosstalk among various signaling pathways, ultimately leading to renal dysfunction and structural injury...
  25. doi request reprint Advanced glycation end-products induce vascular dysfunction via resistance to nitric oxide and suppression of endothelial nitric oxide synthase
    Aino Soro-Paavonen
    JDRF Einstein Centre for Diabetes Complications, Melbourne, Australia
    J Hypertens 28:780-8. 2010
    ....
  26. doi request reprint Circulating high-molecular-weight RAGE ligands activate pathways implicated in the development of diabetic nephropathy
    Sally A Penfold
    Division of Diabetes Complications, Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia
    Kidney Int 78:287-95. 2010
    ..These data show that ligands that activate RAGE present in the circulation of patients with type 2 diabetes and nephropathy are predominantly of high molecular weight...
  27. doi request reprint Glucose homeostasis can be differentially modulated by varying individual components of a western diet
    Josephine M Forbes
    Diabetes Complications, Baker IDI Heart and Diabetes Research Institute, Melbourne, Victoria, Australia
    J Nutr Biochem 24:1251-7. 2013
    ..These data provide clear evidence of a link between over-consumption of a western diet and the development of diabetes...
  28. ncbi request reprint Reduced tubular cation transport in diabetes: prevented by ACE inhibition
    Merlin C Thomas
    Division of Diabetic Complications, Baker Medical Research Institute, Melbourne, Victoria, Australia
    Kidney Int 63:2152-61. 2003
    ..Alterations of cation transport may occur in diabetes, although the role of the OCTs has not been previously assessed...
  29. ncbi request reprint The role of advanced glycation in reduced organic cation transport associated with experimental diabetes
    Merlin C Thomas
    Danielle Alberti Memorial Centre for Diabetes Complications, Baker Medical Research Institute, P O Box 6492, Melbourne, Victoria 8008, Australia
    J Pharmacol Exp Ther 311:456-66. 2004
    ..These changes correlate with the accumulation of AGEs and may be partly attenuated by an AGE inhibitor, implicating a role for AGEs in organic cation transport...
  30. doi request reprint The relationship between heat shock protein 72 expression in skeletal muscle and insulin sensitivity is dependent on adiposity
    Darren C Henstridge
    Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, 3004, Vic, Australia
    Metabolism 59:1556-61. 2010
    ..These findings are consistent with rodent data suggesting that HSP72 stimulates fat oxidation with consequent reduction in fat storage and adiposity...
  31. ncbi request reprint Attenuation of extracellular matrix accumulation in diabetic nephropathy by the advanced glycation end product cross-link breaker ALT-711 via a protein kinase C-alpha-dependent pathway
    Vicki Thallas-Bonke
    Danielle Alberti Memorial Centre for Diabetes Complications, Vascular Division, Baker Medical Research Institute, P O Box 6492, St Kilda Rd Central, Melbourne, Australia
    Diabetes 53:2921-30. 2004
    ..These findings implicate AGEs as important stimuli for the activation of PKC, particularly PKC-alpha, in the diabetic kidney, which can be directly inhibited by ALT-711...
  32. ncbi request reprint Advanced glycation end product interventions reduce diabetes-accelerated atherosclerosis
    Josephine M Forbes
    Danielle Alberti Memorial Centre for Diabetes Complications, Vascular Division, Wynn Domain, Baker Medical Research Institute, Melbourne, Australia
    Diabetes 53:1813-23. 2004
    ..Attenuation of these changes was seen in both treated diabetic groups. ALT-711 and AG demonstrated the ability to reduce vascular AGE accumulation in addition to attenuating atherosclerosis in these diabetic mice...
  33. ncbi request reprint Temporal renal expression of angiogenic growth factors and their receptors in experimental diabetes: role of the renin-angiotensin system
    Bishoy Rizkalla
    Department of Diabetic Complications, Vascular Division, Wynn Domain, Baker Medical Research Institute, Melbourne, Victoria, Australia
    J Hypertens 23:153-64. 2005
    ....
  34. ncbi request reprint Interactions between renin angiotensin system and advanced glycation in the kidney
    Merlin C Thomas
    Baker Medical Research Institute, P O Box 6492, Melbourne, Victoria 8008, Australia
    J Am Soc Nephrol 16:2976-84. 2005
    ..AGE and Ang II have overlapping activities in the kidney. The beneficial effects of blockade of either pathway underline the importance of this interaction in diabetic renal disease and the aging kidney...
  35. doi request reprint Advanced glycation end products (AGEs) are cross-sectionally associated with insulin secretion in healthy subjects
    Josephine M Forbes
    Baker IDI Heart and Diabetes Institute, Melbourne, Australia
    Amino Acids 46:321-6. 2014
    ..39; p < 0.01). In conclusion, in healthy humans, we show a cross-sectional association between advanced glycation end products and acute insulin secretion during glucose tolerance testing...
  36. doi request reprint Insulin infusion reduces hepatocyte growth factor in lean humans
    Barbora de Courten
    Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia
    Metabolism 62:647-50. 2013
    ..The current studies were done to determine if hyperinsulinemia increases plasma HGF...
  37. doi request reprint Mechanisms of diabetic complications
    Josephine M Forbes
    Diabetes Division, Baker IDI Heart and Diabetes Institute, Melbourne, Australia
    Physiol Rev 93:137-88. 2013
    ..In addition, new fields of research, which warrant further investigation as potential therapeutic targets of the future, will be highlighted...
  38. ncbi request reprint Can advanced glycation end product inhibitors modulate more than one pathway to enhance renoprotection in diabetes?
    Melinda T Coughlan
    Danielle Alberti Memorial Centre for Diabetes Complications, Baker Heart Research Institute, P O Box 6492, St Kilda Rd Central, Melbourne 8008, Australia
    Ann N Y Acad Sci 1043:750-8. 2005
    ..Therefore, research into synergistic interactions among the various pathogenic pathways leading to diabetic complications is critical in order to develop interventions that confer optimal end-organ protection...
  39. ncbi request reprint Low-molecular weight advanced glycation end products: markers of tissue AGE accumulation and more?
    Merlin C Thomas
    The Baker Heart Research Institute, P O Box 6492, St Kilda Rd Central, Melbourne, Victoria, Australia
    Ann N Y Acad Sci 1043:644-54. 2005
    ..These findings provide clinical support for the association between AGEs and progressive renal injury in diabetes...
  40. pmc c-Jun NH2-terminal kinase activity in subcutaneous adipose tissue but not nuclear factor-kappaB activity in peripheral blood mononuclear cells is an independent determinant of insulin resistance in healthy individuals
    Karly C Sourris
    Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia
    Diabetes 58:1259-65. 2009
    ..Our study investigated potential relationships between nuclear factor-kappaB (NF-kappaB) and c-Jun NH(2)-terminal kinase (JNK) pathways-two pathways proposed as the link between CLAIS and insulin resistance...
  41. ncbi request reprint Advanced glycation: how are we progressing to combat this web of sugar anomalies in diabetic nephropathy
    Josephine M Forbes
    Danielle Alberti Memorial Centre for Diabetes Complications, Wynn Domain, Vascular Division, Baker Heart Research Institute, Melbourne, Victoria 8008, Australia
    Curr Pharm Des 10:3361-72. 2004
    ....
  42. doi request reprint Oxidative stress and advanced glycation in diabetic nephropathy
    Melinda T Coughlan
    JDRF Albert Einstein Centre for Diabetes Complications, Diabetes and Metabolism Division, Baker Heart Research Institute, Melbourne, Victoria, Australia
    Ann N Y Acad Sci 1126:190-3. 2008
    ..This review focuses on how RAGE and subsequent ROS generation play a deleterious role in the diabetic kidney, promoting cross-talk among signaling pathways, ultimately leading to renal dysfunction...
  43. doi request reprint High-density lipoprotein modulates glucose metabolism in patients with type 2 diabetes mellitus
    Brian G Drew
    Baker IDI Heart and Diabetes Institute, Melbourne, Australia
    Circulation 119:2103-11. 2009
    ..We hypothesized that HDL modulates glucose metabolism via elevation of plasma insulin and through activation of the key metabolic regulatory enzyme, AMP-activated protein kinase, in skeletal muscle...
  44. pmc Modulation of the cellular expression of circulating advanced glycation end-product receptors in type 2 diabetic nephropathy
    Karly C Sourris
    Glycation and Diabetes, Diabetes Division, Baker IDI Heart and Diabetes Institute, Melbourne 3004, Australia
    Exp Diabetes Res 2010:974681. 2010
    ..Advanced glycation end-products (AGEs) and their receptors are prominent contributors to diabetic kidney disease...
  45. ncbi request reprint Advanced glycation: implications in tissue damage and disease
    Anna Gasser
    JDRF Albert Einstein Centre for Diabetes Complications, Baker Heart Research Institute, Melbourne, Australia
    Protein Pept Lett 15:385-91. 2008
    ..Such tissue injury contributes to the development of microvascular complications and is of particular relevance in diabetes where interventions to reduce the accumulation of AGEs is desirable...
  46. ncbi request reprint Advanced glycation end products and diabetic nephropathy
    Merlin C Thomas
    Danielle Alberti Memorial Centre for Diabetes Complications, Baker Medical Research Institute, Melbourne, Victoria, Australia
    Am J Ther 12:562-72. 2005
    ....
  47. doi request reprint Therapeutic interruption of advanced glycation in diabetic nephropathy: do all roads lead to Rome?
    Karly C Sourris
    JDRF Albert Einstein Centre for Diabetes Complications, Diabetes and Metabolism Division, Baker Heart Research Institute, Melbourne, Victoria, Australia
    Ann N Y Acad Sci 1126:101-6. 2008
    ..To understand these novel mechanisms, further examination of the advanced glycation pathway and, in particular, the diverse action of these agents in ameliorating the development of diabetic complications is needed...
  48. ncbi request reprint Interactions between advanced glycation end-products (AGE) and their receptors in the development and progression of diabetic nephropathy - are these receptors valid therapeutic targets
    Karly C Sourris
    Baker IDI Heart and Diabetes Institute, PO Box 6492, St Kilda Rd Central, Melbourne, 8008, Australia
    Curr Drug Targets 10:42-50. 2009
    ..Modulation of AGE receptor expression is an important potential therapeutic approach worth consideration as a treatment for diabetic nephropathy and likely applicable to other vascular complications...
  49. doi request reprint A new perspective on therapeutic inhibition of advanced glycation in diabetic microvascular complications: common downstream endpoints achieved through disparate therapeutic approaches?
    Karly C Sourris
    JDRF Einstein Centre for Diabetes Complications, Diabetes and Metabolism Division, Baker IDI Heart and Diabetes Institute, PO Box 6492 St Kilda Road Central, Melbourne, VIC 8008, Australia
    Am J Nephrol 30:323-35. 2009
    ..These novel actions emphasise the importance of further examination of the advanced glycation pathway and in particular the diverse action of these agents in ameliorating the development of diabetic complications such as nephropathy...
  50. ncbi request reprint Advanced glycation end products as environmental risk factors for the development of type 1 diabetes
    Felicia Y T Yap
    BakerIDI Diabetes and Heart Institute, Melbourne, Victoria, Australia
    Curr Drug Targets 13:526-40. 2012
    ....
  51. ncbi request reprint Role of advanced glycation end products in diabetic nephropathy
    Josephine M Forbes
    Danielle Alberti Memorial Centre for Diabetic Complications, Baker Medical Research Institute, Melbourne, Victoria, Australia
    J Am Soc Nephrol 14:S254-8. 2003
    ..It is likely that therapies that inhibit the formation of AGE will form an important part of future therapy in patients with diabetes, acting synergistically with conventional approaches to prevent diabetic renal injury...
  52. doi request reprint MKK3 signalling plays an essential role in leukocyte-mediated pancreatic injury in the multiple low-dose streptozotocin model
    Kyoichi Fukuda
    Department of Nephrology, Monash Medical Centre, Clayton, Vic, Australia
    Lab Invest 88:398-407. 2008
    ..In conclusion, MKK3 signalling plays an essential role in the development of islet inflammation leading to destruction of beta-cells and hyperglycaemia in MLD-STZ-induced pancreatic injury...
  53. doi request reprint Obesity-induced renal impairment is exacerbated in interleukin-6-knockout mice
    Brooke E Harcourt
    Glycation and Diabetes Complications, Monash University, Melbourne, Victoria, Australia
    Nephrology (Carlton) 17:257-62. 2012
    ..Interleukin-6 (IL-6) is secreted from adipose tissue and thought to contribute to obesity-related disorders. The aim of this study was to assess if IL-6-knockout (IL-6-/-) mice would develop obesity-induced renal impairment...
  54. ncbi request reprint Report on ISN Forefronts, Melbourne, Australia, 4-7 October 2012: tubulointerstitial disease in diabetic nephropathy
    Josephine M Forbes
    1 Mater Medical Research Institute, South Brisbane, Queensland, Australia 2 Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia
    Kidney Int 84:653-6. 2013
    ..The presenters were all extremely generous, giving not only their time, but also showing a large proportion of unpublished data to stimulate discussions, questions and innovation. ..
  55. doi request reprint Effects of high-density lipoprotein elevation with cholesteryl ester transfer protein inhibition on insulin secretion
    Andrew L Siebel
    Baker IDI Heart and Diabetes Institute, Melbourne, Australia
    Circ Res 113:167-75. 2013
    ..High-density lipoprotein cholesterol elevation via cholesteryl ester transfer protein (CETP) inhibition represents a novel therapy for atherosclerosis, which also may have relevance for type 2 diabetes mellitus...
  56. ncbi request reprint Characterization of renal angiotensin-converting enzyme 2 in diabetic nephropathy
    Christos Tikellis
    Department of Medicine, University of Melbourne, Austin and Repatriation Medical Centre, Melbourne, Australia
    Hypertension 41:392-7. 2003
    ....
  57. ncbi request reprint Agents in development for the treatment of diabetic nephropathy
    Kei Fukami
    Danielle Alberti Memorial Centre for Diabetes Complications, Baker Heart Research Institute, PO Box 6492, St Kilda Rd Central, Melbourne, Victoria 8008, Australia
    Expert Opin Investig Drugs 14:279-94. 2005
    ..Such an approach is expected to lead to improved therapies for the treatment of diabetic nephropathy...
  58. ncbi request reprint Reversible angiotensin II-mediated albuminuria in rat kidneys is dynamically associated with cytoskeletal organization
    Steven P Clavant
    Department of Biochemistry and Molecular Biology, Monash University, Clayton, Vic, Australia
    Nephron Physiol 93:p51-60. 2003
    ..These results demonstrate that ANG II may reversibly induce clinical levels of albuminuria. These data point to an important role for renal tubules and the intratubular lumen concentrations of ANG II in the renal processing of albumin...
  59. pmc Below the radar: advanced glycation end products that detour "around the side". Is HbA1c not an accurate enough predictor of long term progression and glycaemic control in diabetes?
    Josephine M Forbes
    Albert Einstein Centre for Diabetes Complications, Baker Heart Research Institute, Monash University, AMREP District, Melbourne, Vic, Australia
    Clin Biochem Rev 26:123-34. 2005
    ..Due to the range of dysfunction produced by the accumulation of AGEs in diabetes, there is a growing need for early recognition and intervention in this process...