Cell-free hemoglobin limits nitric oxide bioavailability in sickle-cell disease
By C. Reiter, Xunde Wang, J. Tanus-Santos, N. Hogg, R. Cannon, A. Schechter, M. Gladwin. Nature Medicine, 2002
848 citations recorded by the source corpus.
Subfields: Cell Biology, Genetics, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/80bbf9611dbe14c7276b2a4dbca6e42007866746
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In Genetics
Citations in the corpus
- Nitrite reduction to nitric oxide by deoxyhemoglobin vasodilates the human circulation (2003, background): “Therapeutic application of nitrite should result in selective vasodilation to hypoxemic tissue, and could be used to treat diseases associated with ischemic tissue, neonatal pulmonary hypertension and hemolytic conditions such as sickle-cell disease, where free hemoglobin released during hemolysis s”
- Arginine metabolism: boundaries of our knowledge. (2007, background): “] Overall, the reduced plasma levels of arginine, together with increased plasma levels of cell-free hemoglobin (which acts as a trap for NO) (86), result in NO insufficiency, consistent with the increased incidence of pulmonary hypertension in sickle cell patients.”
- Mechanisms of cell protection by heme oxygenase-1. (2010, background): “This reaction can have two pathological consequences: (a) reduction of NO bioavailability (161) and (b) Hb oxidation into ferric (Fe3+) Hb, that is, methemoglobin (162, 163), with subsequent release of heme.”