Inhibition of intracellular Angiotensin II formation blocks high glucose effect on mesangial matrix
Author:
Publisher
Elsevier BV
Subject
Cellular and Molecular Neuroscience,Clinical Biochemistry,Endocrinology,Physiology,Biochemistry
Reference19 articles.
1. Angiotensin II and its receptors in the pathogenesis of diabetic nephropathy;Leehey,2006
2. Angiotensin II stimulates extracellular matrix protein synthesis through induction of transforming growth factor-β expression in rat glomerular mesangial cells;Kagami;J Clin Invest,1994
3. Role of angiotensin II in glucose-induced inhibition of mesangial matrix degradation;Singh;Diabetes,1999
4. Mechanism of increased angiotensin II formation in glomerular mesangial cells cultured in high glucose;Singh;J Am Soc Nephrol,2003
5. Glomerular renin angiotensin system in streptozotocin diabetic and Zucker diabetic fatty rats;Leehey;Trans Res,2008
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3. Inhibition of MAPK ‐mediated ACE expression by compound C66 prevents STZ ‐induced diabetic nephropathy;Journal of Cellular and Molecular Medicine;2013-12-11
4. Elevated transcriptional co-activator p102 mediates angiotensin II type 1 receptor up-regulation and extracellular matrix overproduction in the high glucose-treated rat glomerular mesangial cells and isolated glomeruli;European Journal of Pharmacology;2013-02
5. Enzymatic processing of angiotensin peptides by human glomerular endothelial cells;American Journal of Physiology-Renal Physiology;2012-06-15
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