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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Aminoguanidine Ameliorates Overexpression of Prosclerotic Growth Factors and Collagen Deposition in Experimental Diabetic Nephropathy
TL;DR: In this article, the effect of aminoguanidine (1 g/l drinking water) on the tubulointerstitium of Sprague-Dawley rats was investigated.
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Angiotensin Type 2 Receptor Antagonism Confers Renal Protection in a Rat Model of Progressive Renal Injury
Zemin Cao,Fabrice Bonnet,Riccardo Candido,Stefan P. Nesteroff,Wendy C. Burns,Hiroshi Kawachi,Fujio Shimizu,Robert M. Carey,Marc de Gasparo,Mark E. Cooper +9 more
TL;DR: It seems that the combination of the AT(1) and AT(2) receptor antagonists may confer additive renal effects than either receptor antagonist as monotherapy.
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PDGF signal transduction inhibition ameliorates experimental mesangial proliferative glomerulonephritis
Richard E. Gilbert,Darren J. Kelly,Tara Mckay,Steven J. Chadban,Prudence A. Hill,Mark E. Cooper,Robert C. Atkins,David J. Nikolic-Paterson +7 more
TL;DR: The amelioration of the pathological findings of experimental mesangial proliferative glomerulonephritis by blockade of PDGF receptor activity suggests the potential clinical utility of this approach as a therapeutic strategy in glomerular disease.
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The role of the renin-angiotensin-aldosterone system in diabetes and its vascular complications.
TL;DR: Collectively, these studies demonstrate that ATII has direct effects on multiple tissues, and inhibition of ATII action in these tissues may be responsible for many of the clinical benefits observed with RAAS inhibition.
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Metabolic memory and diabetic nephropathy: potential role for epigenetic mechanisms
TL;DR: Preliminary work in endothelial cells has shown that transient episodes of hyperglycemia can induce changes in gene expression that are dependent on modifications to histone tails (for example, methylation), and that these changes persist after return to normoglycemia.