Research Topics
Genomes and Genes | Josephine M ForbesSummaryCountry: Australia Publications
| Collaborators
|
Detail Information
Publications
Glycation in diabetic nephropathyJosephine 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...- Receptor for advanced glycation end-products (RAGE) provides a link between genetic susceptibility and environmental factors in type 1 diabetesJ 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... 
The physiological deadlock between AMPK and gluconeogenesis: SOGA, a novel protein, may provide the keyJosephine 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)...- Disparate effects on renal and oxidative parameters following RAGE deletion, AGE accumulation inhibition, or dietary AGE control in experimental diabetic nephropathyAdeline 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... 
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....- The pleiotropic actions of rosuvastatin confer renal benefits in the diabetic Apo-E knockout mouseSara 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... - Accelerated nephropathy in diabetic apolipoprotein e-knockout mouse: role of advanced glycation end productsMarkus 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... - Preservation of kidney function with combined inhibition of NADPH oxidase and angiotensin-converting enzyme in diabetic nephropathyVicki 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... - Modulation of soluble receptor for advanced glycation end products by angiotensin-converting enzyme-1 inhibition in diabetic nephropathyJosephine 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... - Receptor for advanced glycation end products (RAGE) deficiency attenuates the development of atherosclerosis in diabetesAino 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... - Advanced glycation urinary protein-bound biomarkers and severity of diabetic nephropathy in manMelinda 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... - Ubiquinone (coenzyme Q10) prevents renal mitochondrial dysfunction in an experimental model of type 2 diabetesKarly 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... - Cardiac inflammation associated with a Western diet is mediated via activation of RAGE by AGEsChristos 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... - RAGE-induced cytosolic ROS promote mitochondrial superoxide generation in diabetesMelinda 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.... - Inhibition of NADPH oxidase prevents advanced glycation end product-mediated damage in diabetic nephropathy through a protein kinase C-alpha-dependent pathwayVicki 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... - Connective tissue growth factor plays an important role in advanced glycation end product-induced tubular epithelial-to-mesenchymal transition: implications for diabetic renal diseaseWendy 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... - The breakdown of preexisting advanced glycation end products is associated with reduced renal fibrosis in experimental diabetesJosephine M Forbes
Division of Diabetic Complications, Baker Medical Research Institute, Melbourne, Australia
FASEB J 17:1762-4. 2003.... - Oxidative stress as a major culprit in kidney disease in diabetesJosephine 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.... - Temporal increases in urinary carboxymethyllysine correlate with albuminuria development in diabetesMelinda 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... - Renal microvascular injury in diabetes: RAGE and redox signalingMelinda 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... - Advanced glycation end-products induce vascular dysfunction via resistance to nitric oxide and suppression of endothelial nitric oxide synthaseAino Soro-Paavonen
JDRF Einstein Centre for Diabetes Complications, Melbourne, Australia
J Hypertens 28:780-8. 2010.... - Targeted reduction of advanced glycation improves renal function in obesityBrooke 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... - Reduced tubular cation transport in diabetes: prevented by ACE inhibitionMerlin 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... - The role of advanced glycation in reduced organic cation transport associated with experimental diabetesMerlin 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... - The relationship between heat shock protein 72 expression in skeletal muscle and insulin sensitivity is dependent on adiposityDarren 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... - Advanced glycation end product interventions reduce diabetes-accelerated atherosclerosisJosephine 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... - Interactions between renin angiotensin system and advanced glycation in the kidneyMerlin 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... - Temporal renal expression of angiogenic growth factors and their receptors in experimental diabetes: role of the renin-angiotensin systemBishoy Rizkalla
Department of Diabetic Complications, Vascular Division, Wynn Domain, Baker Medical Research Institute, Melbourne, Victoria, Australia
J Hypertens 23:153-64. 2005.... - Circulating high-molecular-weight RAGE ligands activate pathways implicated in the development of diabetic nephropathySally 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... - Targeting the AGE-RAGE axis improves renal function in the context of a healthy diet low in advanced glycation end-product contentVicki 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... - 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 pathwayVicki 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... - Advanced glycation: how are we progressing to combat this web of sugar anomalies in diabetic nephropathyJosephine 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.... - 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 individualsKarly 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... - 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... - Advanced glycation end products are direct modulators of β-cell functionMelinda 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)... - Modulation of the cellular expression of circulating advanced glycation end-product receptors in type 2 diabetic nephropathyKarly 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... - Oxidative stress and advanced glycation in diabetic nephropathyMelinda 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... - High-density lipoprotein modulates glucose metabolism in patients with type 2 diabetes mellitusBrian 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... - 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... - Advanced glycation: implications in tissue damage and diseaseAnna 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... - Advanced glycation end products and diabetic nephropathyMerlin C Thomas
Danielle Alberti Memorial Centre for Diabetes Complications, Baker Medical Research Institute, Melbourne, Victoria, Australia
Am J Ther 12:562-72. 2005.... - 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... - 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... - Interactions between advanced glycation end-products (AGE) and their receptors in the development and progression of diabetic nephropathy - are these receptors valid therapeutic targetsKarly 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... - Advanced glycation end products as environmental risk factors for the development of type 1 diabetesFelicia Y T Yap
BakerIDI Diabetes and Heart Institute, Melbourne, Victoria, Australia
Curr Drug Targets 13:526-40. 2012.... - Role of advanced glycation end products in diabetic nephropathyJosephine 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... - MKK3 signalling plays an essential role in leukocyte-mediated pancreatic injury in the multiple low-dose streptozotocin modelKyoichi 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... - Obesity-induced renal impairment is exacerbated in interleukin-6-knockout miceBrooke 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... - Reversible angiotensin II-mediated albuminuria in rat kidneys is dynamically associated with cytoskeletal organizationSteven 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... - Characterization of renal angiotensin-converting enzyme 2 in diabetic nephropathyChristos Tikellis
Department of Medicine, University of Melbourne, Austin and Repatriation Medical Centre, Melbourne, Australia
Hypertension 41:392-7. 2003.... - Agents in development for the treatment of diabetic nephropathyKei 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... - 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...