The vascular NAD(P)H oxidases as therapeutic targets in cardiovascular diseases.

By H. Cai, K. Griendling, D. Harrison. TIPS - Trends in Pharmacological Sciences, 2003

737 citations recorded by the source corpus.

Subfields: Cardiology and Cardiovascular Medicine, Physiology

View Paper: https://www.semanticscholar.org/paper/1419691357307cb8829be56b39b2e72fdf5bc19e

How researchers see this paper

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

In Cardiology and Cardiovascular Medicine

1. Rhian M. Touyz
2. E. Schiffrin
3. A. Shah
4. J. Lambeth
5. C. Iadecola
6. S. Dikalov

In Physiology

1. Rhian M. Touyz
2. E. Schiffrin
3. Hélène Girouard
4. A. Shah
5. J. Lambeth
6. C. Iadecola
7. Jian-Mei Li
8. S. Dikalov

Citations in the corpus

• Physiology of local renin-angiotensin systems. (2006, background): “The production of ROS by NAD(P)H oxidase in response to ANG II stimulation in endothelial and vascular smooth muscle cells activates signal pathways such as MAP kinases, tyrosine kinases, and transcription factors that lead to theses events (71, 240, 253, 623).”
• Metabolic oxidation/reduction reactions and cellular responses to ionizing radiation: A unifying concept in stress response biology (2004, background): “NADPH oxidase enzymes are also believed to be mediators of inflammatory injury, mutagenesis, growth disturbances, and transformation in a wide variety of biologically relevant pathologies including tumor promotion and vascular injury as well as normal cell signaling [91–97].”
• Crosstalk between mitochondria and NADPH oxidases (2011, background): “deficient in p47phox and gp91phox NADPH oxidase subunits show that ROS produced by these oxidases contribute to atherosclerosis [134].”
• Neurovascular coupling in the normal brain and in hypertension, stroke, and Alzheimer disease. (2006, background): “ROS are produced by several enzymatic systems (78), but recent findings have identified NADPH oxidase as a major source of ROS at the vascular level (7).”
• Neurovascular regulation in the normal brain and in Alzheimer's disease (2004, background): “But the enzyme NADPH oxidase has emerged as an important source of the ROS that are responsible for vascular dysfunction in other conditions associated with vascular oxidative stress, such as hypertension and hyperhomocysteinaemi”
• Endothelial cell superoxide generation: regulation and relevance for cardiovascular pathophysiology. (2004, background): “Although all the endothelial ROS sources discussed previously may potentially be involved in redox signaling, NADPH oxidases seem to be especially important in that they are the main source whose primary function appears to be to modulate redox signaling (15, 17, 50, 88, 99).”
• Nox enzymes, ROS, and chronic disease: an example of antagonistic pleiotropy. (2007, background): “Nox1 and Nox2 therefore provide promising targets for therapeutic intervention in hypertensive cardiovascular disease [41,78,79].”
• Reactive oxygen species in vascular biology: implications in hypertension (2004, positive): “Gene transfer of GTP cyclohydrolase (GTPCH) I, the enzyme responsible for regenerating BH4, restored arterial GTPCH I activity and BH4 levels, reduced ROS, and improved endotheliumdependent relaxation and NO release in DOCA-salt hypertensive rats, in which endothelial dysfunction results from NAD(P)”