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ECM2 — RENBP

Text-mined interactions from Literome

Vlassara et al., Diabetes 1992 (Diabetes Mellitus...) : Renal mesangial AGE receptors mediate PDGF dependent extracellular matrix protein production
Zhou et al., Am J Pathol 2004 (Diabetic Neuropathies...) : To determine the critical role of CTGF in AGE induced ECM accumulation leading to diabetic nephropathy, rats were given AGEs by intravenous injection for 6 weeks ... AGE treatment induced a significant renal ECM accumulation, as shown by increases in periodic acid-Schiff positive materials, fibronectin, and type IV collagen ( Col IV ) accumulation in glomeruli, and a mild renal dysfunction, as shown by increases in urinary volume and protein content
Ha et al., Nephrology (Carlton) 2005 (Diabetic Nephropathies) : PKC, TGF-beta1, Ang II, and AGE also induce cellular ROS and signal through ROS leading to enhanced ECM synthesis
Yu et al., Toxicological sciences : an official journal of the Society of Toxicology 2007 (Kidney Diseases) : The present study, therefore, was to define whether or not AGE induced renal ECM accumulation and renal dysfunction are mediated by upregulation of PAI-1 expression and whether or not PPAR-gamma agonist can attenuate these AGE effects via suppressing PAI-1 expression ... Treatment with RGZ significantly ameliorated AGE induced renal ECM accumulation, proteinuria, and PAI-1 upregulation ... These results suggest that upregulation of PAI-1 expression plays a critical role in AGE induced renal ECM accumulation
Pugliese et al., Diabetes 1997 : Co-incubation of BSA-AGE with anti-AGE-R1, but not with pre-immune serum, prevented AGE induced increases in IGF-I, TGF-beta1, and ECM production or gene expression ; anti-AGE-R1 also reduced growth factor and matrix synthesis in cells grown on BSA