Inhibition of nitric oxide and antiphospholipid antibody-mediated thrombosis.

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

The antiphospholipid syndrome (APS) is characterized by recurrent vascular thrombosis, thrombocytopenia, and fetal loss occurring in the presence of antiphospholipid antibodies (aPL). Along with arterial and venous thrombosis and pregnancy complications, patients with APS have an increased risk of myocardial infarction, stroke, and coronary artery disease, resulting from vascular cell dysfunction induced by aPL. Accumulating evidence to date indicates that interactions between circulating aPL and cell surface molecules of target cells, primarily endothelial cells and platelets, underlie the vascular disease phenotypes of APS. However, the molecular basis of APS is poorly understood. Nitric oxide produced by endothelial cells is a key determinant of vascular health that regulates several physiologic processes, including thrombosis, endothelial-leukocyte interaction, vascular cell migration, and the modulation of vascular tone. This review will discuss recent findings that indicate a novel mechanism by which aPL antagonize endothelial cell production of nitric oxide and thereby promote thrombosis.

Original languageEnglish (US)
Pages (from-to)324
Number of pages1
JournalCurrent Rheumatology Reports
Volume15
Issue number5
StatePublished - May 2013

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Antiphospholipid Antibodies
Antiphospholipid Syndrome
Blood Vessels
Nitric Oxide
Thrombosis
Endothelial Cells
Pregnancy Complications
Vascular Diseases
Venous Thrombosis
Thrombocytopenia
Cell Movement
Coronary Artery Disease
Leukocytes
Blood Platelets
Stroke
Myocardial Infarction
Phenotype
Health

ASJC Scopus subject areas

  • Rheumatology

Cite this

Inhibition of nitric oxide and antiphospholipid antibody-mediated thrombosis. / Mineo, Chieko.

In: Current Rheumatology Reports, Vol. 15, No. 5, 05.2013, p. 324.

Research output: Contribution to journalArticle

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