Sickle cell disease and nitric oxide: A paradigm shift?

A. Kyle Mack*, Gregory J. Kato

*Corresponding author for this work

Research output: Contribution to journalShort survey

87 Scopus citations

Abstract

Traditionally the pathophysiology of sickle cell disease is thought to result from the polymerization of hemoglobin S in red cells, under hypoxic conditions, resulting in the occlusion of blood vessels. Adhesion of cells to the venular endothelium also appears to play a role. Recent studies have also suggested that in addition to the polymerization of hemoglobin S in the red blood cell, a deficiency of the endogenous vasodilator, nitric oxide may be involved. Hemoglobin released as a result of hemolysis rapidly consumes nitric oxide resulting in a whole program of events that inhibit blood flow. Therapies directed at decreasing the destruction of nitric oxide, increasing the production of nitric oxide, or amplifying the nitric oxide response may prove beneficial.

Original languageEnglish (US)
Pages (from-to)1237-1243
Number of pages7
JournalInternational Journal of Biochemistry and Cell Biology
Volume38
Issue number8
DOIs
Publication statusPublished - May 8 2006

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Keywords

  • Blood flow
  • Nitric oxide
  • Sickle cell

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology

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