Molecular understanding of hyperglycemia's adverse effects for diabetic complications.

By M. Sheetz, G. King. Journal of the American Medical Association (JAMA), 2002

1,065 citations recorded by the source corpus.

Subfields: Clinical Biochemistry, Endocrinology, Diabetes and Metabolism, Neurology

View Paper: https://www.semanticscholar.org/paper/720a140943be280a334b1554f7c11d63553ca3a4

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Clinical Biochemistry

1. R. M. Mason
2. C. van Dijk
3. T. Berl
4. N. Wahab

In Endocrinology, Diabetes and Metabolism

1. Aruni Bhatnagar
2. R. M. Mason
3. Barry M. Popkin
4. C. van Dijk
5. T. Berl
6. N. Wahab

In Neurology

1. R. M. Mason
2. C. van Dijk
3. T. Berl
4. N. Wahab

Citations in the corpus

• Role of aldose reductase and oxidative damage in diabetes and the consequent potential for therapeutic options. (2005, background): “Because AR utilizes NADPH to catalyze glucose reduction, we, as well as other investigators, suggested that tissue injury associated with high glucose may be due, in part, to increased NADPH utilization by the reduction of glucose by AR (24, 25).”
• Individuals with obesity and COVID‐19: A global perspective on the epidemiology and biological relationships (2020, background): “times of infection, uncontrolled serum glucose can impair immune cell function either directly or indirectly via generation of oxidants and glycation products.(117) Similarly, both insulin and leptin signalling are critical in the inflammatory effector response of T cells by upregulating cellular gl”
• Extracellular matrix metabolism in diabetic nephropathy. (2003, positive): “The details of activation of these four pathways in high glucose have been reviewed extensively recently (94,95).”
• Oxidative stress and reactive oxygen species in endothelial dysfunction associated with cardiovascular and metabolic diseases. (2018, background): “AC C EP TE D M AN U SC R IP T overexpression of adhesion molecules, increase in ET-1 release [124], and activation of p66 Shc [125,”
• Pathogenesis of Diabetic Nephropathy (2004, positive): “This has been mainly attributed to dose-limiting side effects or inability to achieve adequate tissue levels of drug but may imply that AR is not the single predominant enzyme involved in the intricate pathways that lead to DMN but rather contributes to the early pathogenesis in the presence of hype”
• Vascular endothelial growth factor in eye disease. (2008, background): “3.7.2 Inhibiting PKC—Preclinical studies have provided strong evidence implicating the activation of PKCβ in the upregulation of VEGF expression during diabetic retinopathy (for review, see Sheetz and King, 2002).”