Karly C Sourris
- 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...
- 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...
- Receptor for AGEs (RAGE) blockade may exert its renoprotective effects in patients with diabetic nephropathy via induction of the angiotensin II type 2 (AT2) receptorK C Sourris
JDRF Einstein Centre for Diabetes Complications, Baker Heart Research Institute, PO Box 6492, St Kilda Rd Central, Melbourne, Victoria, 8008, Australia
Diabetologia 53:2442-51. 2010..In this study, we examined whether the protective effects of RAGE blockade are exerted via modulation of the renal angiotensin II type 2 (AT2) receptor...
- 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...
- 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...
- 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...
- 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....
- 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...
- 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...
- Deficiency in mitochondrial complex I activity due to Ndufs6 gene trap insertion induces renal diseaseJosephine 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...
- 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...
- 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...
- 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...