The Pathobiology of Diabetic Complications
Top Cited Papers
- 1 June 2005
- journal article
- Published by American Diabetes Association in Diabetes
- Vol. 54 (6), 1615-1625
- https://doi.org/10.2337/diabetes.54.6.1615
Abstract
No abstract availableThis publication has 55 references indexed in Scilit:
- Matrix protein glycation impairs agonist‐induced intracellular Ca2+ signaling in endothelial cellsJournal of Cellular Physiology, 2002
- Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33)The Lancet, 1998
- High glucose-induced transforming growth factor beta1 production is mediated by the hexosamine pathway in porcine glomerular mesangial cells.JCI Insight, 1998
- Characterization of protein kinase C beta isoform activation on the gene expression of transforming growth factor-beta, extracellular matrix components, and prostanoids in the glomeruli of diabetic rats.JCI Insight, 1997
- Glucose Metabolism to Glucosamine Is Necessary for Glucose Stimulation of Transforming Growth Factor-α Gene TranscriptionPublished by Elsevier BV ,1996
- Amelioration of Vascular Dysfunctions in Diabetic Rats by an Oral PKC β InhibitorScience, 1996
- Advanced glycation endproducts interacting with their endothelial receptor induce expression of vascular cell adhesion molecule-1 (VCAM-1) in cultured human endothelial cells and in mice. A potential mechanism for the accelerated vasculopathy of diabetes.JCI Insight, 1995
- Receptor-specific induction of insulin-like growth factor I in human monocytes by advanced glycosylation end product-modified proteins.JCI Insight, 1992
- Human and rat mesangial cell receptors for glucose-modified proteins: potential role in kidney tissue remodelling and diabetic nephropathy.The Journal of Experimental Medicine, 1991
- Cachectin/TNF and IL-1 Induced by Glucose-Modified Proteins: Role in Normal Tissue RemodelingScience, 1988