Inflammatory mediators of endothelial injury in sickle cell disease

Hematol Oncol Clin North Am. 2014 Apr;28(2):265-86. doi: 10.1016/j.hoc.2013.11.006. Epub 2014 Jan 18.

Abstract

Inflammation plays a critical role in the complex pathophysiology of sickle cell disease and drives both the acute and chronic processes leading to vascular injury. Mediators of inflammation, such as cellular adhesion molecules, cytokines, leukotrienes, and nuclear factor κB signaling factors, represent potential therapeutic targets in sickle cell disease.

Keywords: Inflammation; Mediators; Sickle cell.

Publication types

  • Review

MeSH terms

  • Anemia, Sickle Cell / drug therapy
  • Anemia, Sickle Cell / metabolism*
  • Anemia, Sickle Cell / physiopathology
  • Cell Adhesion Molecules / antagonists & inhibitors
  • Cell Adhesion Molecules / metabolism
  • Cytokines / antagonists & inhibitors
  • Cytokines / metabolism
  • Endothelium, Vascular / drug effects
  • Endothelium, Vascular / metabolism*
  • Endothelium, Vascular / physiopathology
  • Humans
  • Inflammation / drug therapy
  • Inflammation / metabolism*
  • Inflammation / physiopathology
  • Inflammation Mediators / antagonists & inhibitors
  • Inflammation Mediators / metabolism*
  • Leukotrienes / metabolism
  • Molecular Targeted Therapy / methods
  • NF-kappa B / antagonists & inhibitors
  • NF-kappa B / metabolism
  • Signal Transduction / drug effects

Substances

  • Cell Adhesion Molecules
  • Cytokines
  • Inflammation Mediators
  • Leukotrienes
  • NF-kappa B