Sickle cell vaso-occlusion

Elaine Y. Chiang, Paul S. Frenette

Research output: Contribution to journalArticle

94 Citations (Scopus)

Abstract

The vaso-occlusion model has evolved impressively over the past several decades from polymerization-based concepts to a complex, wide-ranging schema that involves multistep, heterogeneous, and interdependent interactions among sickle erythrocytes (SSRBCs), adherent leukocytes, endothelial cells, plasma proteins, and other factors. Endothelial activation, induced directly or indirectly by the proinflammatory behavior of SSRBCs, is the most likely initiating step toward vaso-occlusion. Given the complexity and dynamic relationships of the potential mechanisms leading to vaso-occlusion, further in vivo studies in relevant sickle cell animal models will most likely yield the greatest advances and promote the development of novel, more effective therapeutic strategies.

Original languageEnglish (US)
Pages (from-to)771-784
Number of pages14
JournalHematology/Oncology Clinics of North America
Volume19
Issue number5
DOIs
StatePublished - Oct 2005
Externally publishedYes

Fingerprint

Polymerization
Blood Proteins
Leukocytes
Endothelial Cells
Animal Models
Erythrocytes
Therapeutics

ASJC Scopus subject areas

  • Oncology
  • Hematology

Cite this

Sickle cell vaso-occlusion. / Chiang, Elaine Y.; Frenette, Paul S.

In: Hematology/Oncology Clinics of North America, Vol. 19, No. 5, 10.2005, p. 771-784.

Research output: Contribution to journalArticle

Chiang, Elaine Y. ; Frenette, Paul S. / Sickle cell vaso-occlusion. In: Hematology/Oncology Clinics of North America. 2005 ; Vol. 19, No. 5. pp. 771-784.
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