Novel Competitive Inhibitor of NAD(P)H Oxidase Assembly Attenuates Vascular O2− and Systolic Blood Pressure in Mice

By F. Rey, M. Cifuentes, A. Kiarash, M. Quinn, P. Pagano. Circulation Research, 2001

650 citations recorded by the source corpus.

Subfields: Biochemistry, Physiology

View Paper: https://www.semanticscholar.org/paper/6954f93c1057aef2499f3d1305e399ffa76cbf7d

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In Biochemistry

1. A. Shah
2. Jian-Mei Li
3. Rhian M. Touyz
4. R. Clempus
5. B. Lassègue

In Physiology

1. Rhian M. Touyz
2. R. Clempus
3. A. Shah
4. T. Paravicini
5. B. Lassègue
6. Jian-Mei Li
7. T. Guzik
8. E. Schiffrin

Citations in the corpus

• Vascular NAD(P)H oxidases: specific features, expression, and regulation. (2003, background): “The relationship between superoxide and hypertension was studied in animal models in which blood pressure is elevated by diverse mechanisms, including 1) long-term infusion of subpressor doses of vasoconstrictor agonists, such as ANG II (18, 32, 54, 103, 133, 140, 143, 153, 155, 209, 211) or norepin”
• NADPH Oxidases in Cardiovascular Health and Disease (2006, background): “In short-term Ang II-induced hypertension in mice, the infusion of a peptide inhibitor of NADPH oxidase attenuated the rise in blood pressure (286).”
• Redox signaling in hypertension. (2006, background): “In rats made hypertensive by Ang II infusion, both NAD(P)H oxidase subunit expression and activity are increased [9,30], whilst administration of a NAD(P)H oxidase inhibitor reduces vascular O2 & production and attenuates Ang II-induced increases in blood pressure [31].”
• Endothelial cell superoxide generation: regulation and relevance for cardiovascular pathophysiology. (2004, background): “Studies in hypertensive models associated with activation of the renin-angiotensin system have convincingly shown that increased NADPH oxidase activity (at least in part due to increased subunit expression) contributes both to endothelial dysfunction and elevation of blood pressure per se (21, 50, 8”
• Nitric oxide and superoxide in inflammation and immune regulation. (2003, methodology): “Apocynin, an NAD(P)H oxidase activation inhibitor has been successfully used in limiting inflammation in animal model of rheumatoid arthritis (73, 74), while decoy peptide, which prevents an association of NAD(P)H oxidase subunits was shown to be effective in inflammation related to atherosclerosis ”
• Nox family NADPH oxidases: Molecular mechanisms of activation. (2014, neutral): “The plant component celastrol acts as inhibitor of Nox activation by blocking the interaction of Nox1 and Nox2 with the cytosolic components [295].”