Novel gp91phox Homologues in Vascular Smooth Muscle Cells: nox1 Mediates Angiotensin II-Induced Superoxide Formation and Redox-Sensitive Signaling Pathways

By B. Lassègue, D. Sorescu, K. Szöcs, Qiqin Yin, M. Akers, Yong Zhang, S. Grant, J. Lambeth, K. Griendling. Circulation Research, 2001

919 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/8dd4a73c013c1556afefe0b6d7b26dc3dd24dd36

How researchers see this paper

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

In Immunology

1. Rhian M. Touyz
2. E. Schiffrin
3. K. Griendling
4. B. Lassègue
5. J. Lambeth
6. R. Clempus
7. David I. Brown
8. T. Paravicini

In Molecular Biology

1. Rhian M. Touyz
2. E. Schiffrin
3. K. Griendling
4. David I. Brown
5. A. Shah
6. J. Lambeth
7. M. Wolin
8. P. Mehta

In Physiology

1. Rhian M. Touyz
2. E. Schiffrin
3. K. Griendling
4. J. Lambeth
5. B. Lassègue
6. R. Clempus
7. U. Förstermann
8. A. Shah

Citations in the corpus

• Combating oxidative stress in vascular disease: NADPH oxidases as therapeutic targets (2011, background): “; VSMCs express NOX1 oxidase, NOX4 oxidase and NOX5 oxidas”
• NADPH Oxidases in Cardiovascular Health and Disease (2006, methodology): “By contrast, Nox4 mRNA is downregulated by thrombin and interleukin-1 (90) but upregulated by human urotensin II (77) and 7-ketocholesterol (272), whereas the effects of Ang II and serum are conflicting (356, 191).”
• Redox signaling in hypertension. (2006, background): “Ang II-stimulated ROS production and p38MAP kinase activation were prevented by antisense to either p22phox or Nox1, membrane-bound subunits of NAD(P)H oxidase [77,81].”
• Reactive oxygen species in vascular biology: implications in hypertension (2004, positive): “Nox4 appears to be abundantly expressed in all vascular cell types (Wingler et al. 2001; Yamawaki et al. 2003) and may play an important role in constitutive production of ·O2 in non-proliferating cells (Lassegue et al. 2001; Wingler et al. 2001).”
• Vascular NAD(P)H oxidases: specific features, expression, and regulation. (2003, methodology): “Although the vascular enzyme is activated within minutes of stimulation (107, 168, 231), its activity can also be markedly upregulated in the hours after exposure to agonists.”
• Vascular oxidative stress, nitric oxide and atherosclerosis. (2014, background): “The activity of Nox4 relies on its association with p22phox, whereas the activity of Nox1 and Nox2 in vascular cells requires not only p22phox but also p47phox (or NOXO1), p67phox (or NOXA1) and Rac1 [32].”