V. Thallas‐Bonke

发表

Deficiency in Apoptosis-Inducing Factor Recapitulates Chronic Kidney Disease via Aberrant Mitochondrial Homeostasis

Merlin C. Thomas, Merlin C Thomas, R. MacIsaac, 2016, Diabetes.

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

H. Schmidt, M. Cooper, G. Ramm, 2016, Diabetologia.

Tandem Inhibition of PKC in Di ab etic Nephropathy It Takes Two to Tango?

M. Cooper, V. Thallas‐Bonke, M. Cooper, 2013 .

Modulation of soluble receptor for advanced glycation end products by angiotensin-converting enzyme-1 inhibition in diabetic nephropathy.

Merlin C. Thomas, Merlin C Thomas, G. Jerums, 2005, Journal of the American Society of Nephrology : JASN.

A developmental nephron deficit in rats is associated with increased susceptibility to a secondary renal injury due to advanced glycation end-products

J. Forbes, M. Black, K. Denton, 2006, Diabetologia.

Advanced Glycation End Products Are Direct Modulators of b -Cell Function

M. Knip, P. Groop, B. Kingwell, 2011 .

Combination therapy with the advanced glycation end product cross-link breaker, alagebrium, and angiotensin converting enzyme inhibitors in diabetes: synergy or redundancy?

M. Cooper, D. M. Long, J. Forbes, 2007, Endocrinology.

Response to Comment on: Thallas-Bonke et al. (2008) Inhibition of NADPH Oxidase Prevents Advanced Glycation End Product–Mediated Damage in Diabetic Nephropathy Through a Protein Kinase C-α–Dependent Pathway: Diabetes 57:460–469, 2008

J. Forbes, V. Thallas‐Bonke, 2008, Diabetes.

Disparate effects on renal and oxidative parameters following RAGE deletion, AGE accumulation inhibition, or dietary AGE control in experimental diabetic nephropathy.

Merlin C. Thomas, Merlin C Thomas, M. Cooper, 2010, American journal of physiology. Renal physiology.

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.

M. Cooper, H. Haller, J. Forbes, 2004, Diabetes.

Advanced glycation: how are we progressing to combat this web of sugar anomalies in diabetic nephropathy.

Merlin C. Thomas, Merlin C Thomas, M. Cooper, 2004, Current pharmaceutical design.

Connective tissue growth factor plays an important role in advanced glycation end product-induced tubular epithelial-to-mesenchymal transition: implications for diabetic renal disease.

Merlin C. Thomas, Merlin C Thomas, M. Cooper, 2006, Journal of the American Society of Nephrology : JASN.

RAGE-induced cytosolic ROS promote mitochondrial superoxide generation in diabetes.

M. Cooper, K. Sourris, M. Brownlee, 2009, Journal of the American Society of Nephrology : JASN.

Targeted deletion of NADPH-Oxidase Nox4 from proximal tubules is dispensable for diabetic kidney disease development.

A. Shah, M. Cooper, K. Sourris, 2020, Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association.

Ramipril inhibits AGE-RAGE-induced matrix metalloproteinase-2 activation in experimental diabetic nephropathy

M. Cooper, J. Forbes, V. Thallas-Bonke, 2014, Diabetology & Metabolic Syndrome.

NADPH Oxidase Nox5 Accelerates Renal Injury in Diabetic Nephropathy

D. Power, R. Touyz, M. Cooper, 2017, Diabetes.

Dedifferentiation of Immortalized Human Podocytes in Response to Transforming Growth Factor-β

Merlin C. Thomas, Merlin C Thomas, M. Cooper, 2011, Diabetes.

Inhibition of NADPH Oxidase Prevents Advanced Glycation End Product–Mediated Damage in Diabetic Nephropathy Through a Protein Kinase C-α–Dependent Pathway

M. Cooper, K. Sourris, J. Forbes, 2008, Diabetes.

AT2R Agonist, Compound 21, Is Reno-Protective Against Type 1 Diabetic Nephropathy

Merlin C. Thomas, Merlin C Thomas, M. Cooper, 2015, Hypertension.

Targeting the AGE‐RAGE axis improves renal function in the context of a healthy diet low in advanced glycation end‐product content

M. Cooper, J. Forbes, V. Thallas-Bonke, 2013, Nephrology.

Complement C5a Induces Renal Injury in Diabetic Kidney Disease by Disrupting Mitochondrial Metabolic Agility

P. Meikle, R. MacIsaac, D. Power, 2019, Diabetes.

Advanced Glycation End Products Are Direct Modulators of β-Cell Function

M. Knip, J. Miyazaki, P. Groop, 2011, Diabetes.

Delineating a role for the Mitochondrial Permeability Transition Pore in Diabetic Kidney Disease by targeting Cyclophilin D.

M. Cooper, J. Forbes, Tuong-Vi Nguyen, 2020, Clinical science.

Genetic targeting or pharmacologic inhibition of NADPH oxidase nox4 provides renoprotection in long-term diabetic nephropathy.

R. Touyz, H. Schmidt, M. Cooper, 2014, Journal of the American Society of Nephrology : JASN.

Globally elevating the AGE clearance receptor, OST48, does not protect against the development of diabetic kidney disease, despite improving insulin secretion

K. Sourris, B. Schulz, J. Forbes, 2019, Scientific Reports.

Processed foods drive intestinal barrier permeability and microvascular diseases

C. Mackay, M. Cooper, T. Woodruff, 2021, Science Advances.

Nox-4 and progressive kidney disease

M. Cooper, K. Jandeleit-Dahm, V. Thallas‐Bonke, 2015, Current opinion in nephrology and hypertension.

Targeting Methylglyoxal in Diabetic Kidney Disease Using the Mitochondria-Targeted Compound MitoGamide

M. Cooper, A. El-Osta, R. Hartley, 2021, Nutrients.

Targeted reduction of advanced glycation improves renal function in obesity.

Merlin C. Thomas, M. Cooper, B. Kingwell, 2011, Kidney international.

Mapping time-course mitochondrial adaptations in the kidney in experimental diabetes.

M. Cooper, K. Sourris, J. Forbes, 2016, Clinical science.

Lack of the Antioxidant Enzyme Glutathione Peroxidase-1 Accelerates Atherosclerosis in Diabetic Apolipoprotein E–Deficient Mice

I. Kola, M. Cooper, J. D. de Haan, 2007, Circulation.

Preservation of Kidney Function with Combined Inhibition of NADPH Oxidase and Angiotensin-Converting Enzyme in Diabetic Nephropathy

M. Cooper, J. Forbes, V. Thallas-Bonke, 2010, American Journal of Nephrology.

Nox‐4 deletion reduces oxidative stress and injury by PKC‐α‐associated mechanisms in diabetic nephropathy

H. Schmidt, M. Cooper, H. Haller, 2014, Physiological reports.

NADPH Oxidase Nox5 Accelerates Renal Injury in Diabetic Nephropathy

D. Power, R. Touyz, J. Jha, 2017, Diabetes.

Tandem Inhibition of PKC in Diαβetic Nephropathy

V. Thallas‐Bonke, M. Cooper, 2013, Diabetes.