TY - JOUR
T1 - Inhibition of nitric oxide and antiphospholipid antibody-mediated thrombosis topical collection on antiphospholipid syndrome
AU - Mineo, Chieko
N1 - Funding Information:
Acknowledgments Chieko Mineo has received grant support from the Alliance for Lupus Research and the National Institutes of Health.
PY - 2013/5
Y1 - 2013/5
N2 - 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.
AB - 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.
KW - Antiphospholipid syndrome
KW - Apolipoprotein E receptor 2
KW - Endothelial nitric oxide synthase
KW - Endothelium
KW - Nitric oxide
KW - Nitric oxide inhibition
KW - Platelets
KW - Thrombosis
KW - β2-glycoprotein I
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U2 - 10.1007/s11926-013-0324-4
DO - 10.1007/s11926-013-0324-4
M3 - Article
C2 - 23519891
AN - SCOPUS:84886456636
SN - 1523-3774
VL - 15
JO - Current Rheumatology Reports
JF - Current Rheumatology Reports
IS - 5
M1 - 324
ER -