TY - JOUR
T1 - Inducible nitric oxide synthase and vascular injury
AU - Kibbe, Melina
AU - Billiar, Timothy
AU - Tzeng, Edith
N1 - Funding Information:
Supported by the National Institutes of Health grant GM44100 (T.R. Billiar) and HL-57854 (E. Tzeng). Melina Kibbe is also a recipient of the Ethicon–Society of University Surgeons Resident Research Fellowship.
PY - 1999/8/15
Y1 - 1999/8/15
N2 - The role nitric oxide (NO) plays in the cardiovascular system is complex and diverse. Even more controversial is the role that the inducible NO synthase enzyme (iNOS) serves in mediating different aspects of cardiovascular pathophysiology. Following arterial injury, NO has been shown to serve many vasoprotective roles, including inhibition of platelet aggregation and adherence to the site of injury, inhibition of leukocyte adherence, inhibition of vascular smooth muscle cell (VSMC) proliferation and migration, and stimulation of endothelial cell (EC) growth. These properties function together to preserve a normal vascular environment following injury. In this review, we discuss what is known about the involvement of iNOS in the vascular injury response. Additionally, we discuss the beneficial role of iNOS gene transfer to the vasculature in preventing the development of neointimal thickening. Lastly, the pathophysiology of transplant vasculopathy is discussed as well as the role of iNOS in this setting.
AB - The role nitric oxide (NO) plays in the cardiovascular system is complex and diverse. Even more controversial is the role that the inducible NO synthase enzyme (iNOS) serves in mediating different aspects of cardiovascular pathophysiology. Following arterial injury, NO has been shown to serve many vasoprotective roles, including inhibition of platelet aggregation and adherence to the site of injury, inhibition of leukocyte adherence, inhibition of vascular smooth muscle cell (VSMC) proliferation and migration, and stimulation of endothelial cell (EC) growth. These properties function together to preserve a normal vascular environment following injury. In this review, we discuss what is known about the involvement of iNOS in the vascular injury response. Additionally, we discuss the beneficial role of iNOS gene transfer to the vasculature in preventing the development of neointimal thickening. Lastly, the pathophysiology of transplant vasculopathy is discussed as well as the role of iNOS in this setting.
KW - Inducible nitric oxide synthase
KW - Nitric oxide
KW - Vascular injury
KW - Vasoprotection
UR - http://www.scopus.com/inward/record.url?scp=0033567070&partnerID=8YFLogxK
U2 - 10.1016/S0008-6363(99)00130-3
DO - 10.1016/S0008-6363(99)00130-3
M3 - Review article
C2 - 10690336
AN - SCOPUS:0033567070
SN - 0008-6363
VL - 43
SP - 650
EP - 657
JO - Cardiovascular Research
JF - Cardiovascular Research
IS - 3
ER -