M
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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Journal ArticleDOI
Apoptosis and angiotensin II: yet another renal regulatory system?
TL;DR: Recent studies suggest that both AT1 and AT2 receptors influence the apoptotic process in the kidney, and angiotensin II should be considered as representing another regulatory mechanism that may modulate the balance between cell growth and proliferation within the kidney.
Book ChapterDOI
Complexity, quantitative traits and plant breeding: a role for simulation modelling in the genetic improvement of crops
Journal ArticleDOI
Calcium channel blockers, either amlodipine or mibefradil, ameliorate renal injury in experimental diabetes
TL;DR: Calcium channel blockers attenuated albuminuria, pathologic injury, and accumulation of extracellular matrix proteins in this normotensive model of diabetic nephropathy suggest that CCBs may be useful in preventing pathologic injuries in the diabetic kidney.
Journal ArticleDOI
The pleiotropic actions of rosuvastatin confer renal benefits in the diabetic Apo-E knockout mouse
Sara Giunti,Anna C. Calkin,Josephine M. Forbes,Terri J. Allen,Terri J. Allen,Merlin C. Thomas,Merlin C. Thomas,Mark E. Cooper,Karin Jandeleit-Dahm +8 more
TL;DR: In the diabetic Apo-E(-/-) mouse, rosuvastatin confers renal benefits that are independent of lipid lowering and equivalent or greater to those observed with candesartan, and the combination treatment is not superior to monotherapies.
Journal ArticleDOI
The angiotensin II type 2 receptor agonist Compound 21 is protective in experimental diabetes-associated atherosclerosis.
Bryna S.M. Chow,Christine Koulis,Pooja Krishnaswamy,Ulrike Muscha Steckelings,Thomas Unger,Mark E. Cooper,Karin Jandeleit-Dahm,Terri J. Allen +7 more
TL;DR: C21 treatment significantly attenuated aortic plaque deposition in a mouse model of DAA in vivo, in association with a decreased infiltration of macrophages and mediators of inflammation, oxidative stress and fibrosis, and these atheroprotective actions of C21 were completely blocked by the AT2R antagonist PD123319.