Intermittent high glucose enhances apoptosis related to oxidative stress in human umbilical vein endothelial cells: the role of protein kinase C and NAD(P)H-oxidase activation.

By L. Quagliaro, L. Piconi, R. Assaloni, L. Martinelli, E. Motz, Antonio Ceriello. Diabetes, 2003

801 citations recorded by the source corpus.

Subfields: Molecular Biology, Ophthalmology, Physiology

View Paper: https://www.semanticscholar.org/paper/8438db5971248bc7584c6d80cd2a76845973e4a7

How researchers see this paper

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

In Molecular Biology

1. Antonio Ceriello

In Physiology

1. Antonio Ceriello
2. F. Cosentino
3. Joshua A. Beckman
4. F. Paneni
5. M. Creager

Citations in the corpus

• Glycemic variability: A strong independent predictor of mortality in critically ill patients* (2008, background): “The levels of protein kinase C-beta were significantly higher following alternating glycemia levels than following sustained hyperglycemia (24).”
• The role of oxidative stress in diabetic complications (2007, background): “vascular endothelial cells (37,38), colonic”
• Diabetes and vascular disease: pathophysiology, clinical consequences, and medical therapy: part I (2013, background): “Indeed, treatment with a PKCb inhibitor suppresses NADPHdependent ROS generation.(16) More recently, it has been reported that glucose-induced activation of PKC b2 isoform phosphorylates p66 Shc at serine 36 leading to its translocation to the mitochondria, cytochrome c oxidation and accumulation of”
• Oscillating Glucose Is More Deleterious to Endothelial Function and Oxidative Stress Than Mean Glucose in Normal and Type 2 Diabetic Patients (2008, background): “Studies in cells and in animals, however, have shown that in oscillating glucose pathways involving protein kinase C (22), NADPH (22), inducible nitric oxide synthase (27), or inflammatory markers are more activated in response to oscillating glucose compared with constant high glucose (23–25).”
• Diabetes and Vascular Disease: Pathophysiology, Clinical Consequences, and Medical Therapy: Part I (2003, background): “Indeed, treatment with a PKCb inhibitor suppresses NADPHdependent ROS generation.(16) More recently, it has been reported that glucose-induced activation of PKC b2 isoform phosphorylates p66 Shc at serine 36 leading to its translocation to the mitochondria, cytochrome c oxidation and accumulation of”