Redistribution of Intracellular Oxygen in Hypoxia by Nitric Oxide: Effect on HIF1α

By T. Hagen, Cormac T. Taylor, Francis Lam, S. Moncada. Science, 2003

745 citations recorded by the source corpus.

Subfields: Cancer Research, Genetics, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/f5953d69ad53532f790cbe99aea42b8908f9830e

How researchers see this paper

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

In Cancer Research

1. G. Semenza
2. Navdeep S. Chandel
3. M. C. Simon
4. P. Schumacker
5. Craig B. Thompson
6. P. Ratcliffe
7. W. Kaelin
8. Eyal Gottlieb

In Genetics

1. G. Semenza
2. Navdeep S. Chandel
3. M. C. Simon
4. P. Schumacker
5. R. Guzy
6. W. Kaelin
7. P. Ratcliffe
8. Craig B. Thompson

In Molecular Biology

1. G. Semenza
2. Navdeep S. Chandel
3. P. Schumacker
4. M. C. Simon
5. W. Kaelin
6. P. Ratcliffe
7. Craig B. Thompson
8. Eyal Gottlieb

Citations in the corpus

• Mitochondrial complex III is required for hypoxia-induced ROS production and cellular oxygen sensing. (2005, background): “, 2003), so it has been proposed that PHDs function as O2 sensors because the decreasing availability of O2 during hypoxia could limit their ability to hydroxylate HIF (Hagen et al., 2003; Epstein et al., 2001).”
• The discovery of nitric oxide and its role in vascular biology (2006, background): “…demonstrated that the inhibitory action of NO on oxygen consumption in the mitochondria has the further consequence of diverting oxygen British Journal of Pharmacology vol 147 (S1) away from the mitochondria to other areas of the cell and probably to surrounding tissues (Hagen et al., 2003).”
• ADAPTIVE AND MALADAPTIVE CARDIORESPIRATORY RESPONSES TO CONTINUOUS AND INTERMITTENT HYPOXIA MEDIATED BY HYPOXIA-INDUCIBLE FACTORS 1 AND 2 (2012, background): “However, it should be noted that other investigators have reported that inhibitors of any of the ETC complexes will inhibit the hypoxia-induced stabilization of HIF-1 and that they do so by reducing mitochondrial O2 consumption, thereby facilitating prolyl hydroxylation (49, 73, 108).”
• Mitochondrial dysfunction resulting from loss of cytochrome c impairs cellular oxygen sensing and hypoxic HIF-alpha activation. (2005, neutral): “It is possible that increased O2 availability in the respiratorydeficient cytochrome c null cells accounts for differences in sensitivity to hypoxia, similar to that recently reported with nitric oxide-mediated (NO) mitochondrial inhibition (Hagen et al., 2003).”
• Redox Regulation of Cell Survival (2008, neutral): “(108).”
• Oxygen sensing requires mitochondrial ROS but not oxidative phosphorylation. (2005, background): “Recent data also suggest that mitochondria play a role in oxygen sensing not by increasing the generation of ROS during hypoxia, but through mitochondrial respiration regulating intracellular oxygen levels (Hagen et al., 2003).”
• Dietary nitrate supplementation reduces the O2 cost of low-intensity exercise and enhances tolerance to high-intensity exercise in humans. (2009, background): “The NO so produced is capable of diffusion and may inhibit mitochondrial O2 consumption in the myocytes proximal to the capillary bed, promoting deeper diffusion of the available O2 (32, 59) and, therefore, enabling a more appropriate matching of local O2 delivery to O2 requirement.”