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Mark E. Cooper

Researcher at University of Queensland

Publications -  1514
Citations -  141899

Mark E. Cooper is an academic researcher from University of Queensland. The author has contributed to research in topics: Diabetes mellitus & Diabetic nephropathy. The author has an hindex of 158, co-authored 1463 publications receiving 124887 citations. Previous affiliations of Mark E. Cooper include University of Cambridge & University of Adelaide.

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Dicarbonyl stress in the absence of hyperglycemia increases endothelial inflammation and atherogenesis similar to that observed in diabetes.

TL;DR: It is demonstrated that increasing plasma MG to levels observed in diabetic mice either using an exogenous source or generated following inhibition, its primary clearance enzyme, glyoxalase-1, was able to increase vascular adhesion and augment atherogenesis in euglycemic apolipoprotein E knockout mice to a similar magnitude as that observed in hyperglycemic mice with diabetes.
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Retinal Expression of Vascular Endothelial Growth Factor Is Mediated by Angiotensin Type 1 and Type 2 Receptors

TL;DR: It is suggested that VEGF expression is modulated by AT1 and AT2 receptors, thereby implicating angiotensin II receptor subtypes in retinal diseases such as diabetic retinopathy.
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Diabetes-Associated Mesenteric Vascular Hypertrophy Is Attenuated by Angiotensin-Converting Enzyme Inhibition

TL;DR: ACE inhibition may have a specific role in preventing diabetes-associated vascular hypertrophy, an important process in the genesis of micro- and macrovascular diabetic complications.
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Endothelin Receptor Antagonism Ameliorates Mast Cell Infiltration, Vascular Hypertrophy, and Epidermal Growth Factor Expression in Experimental Diabetes

TL;DR: It is suggested that endogenous endothelin and EGF may play a role in diabetes-induced vascular hypertrophy and that mast cells may be pathogenetically involved in this process.