Inducible nitric oxide synthase may play a protective role against atherosclerosis and restenosis, highlighting NO donors and gene transfer as potential therapies.
iNOS upregulation in lesions is hypothesis-generating; leaves open whether NO donors or gene therapy alter atherosclerosis or restenosis.
Nitric oxide (NO) synthase induction in vascular smooth muscle cells may play a role in local vascular injury associated with atherosclerosis or postangioplasty restenosis by inhibiting smooth muscle cell proliferation and contraction, as well as by preventing leukocyte and platelet adhesion. The expression of inducible NO synthase is increased in balloon-injured arteries of experimental animals or in human atherosclerotic lesions. Replacement therapy with NO donors or NO synthase gene transfer may improve the clinical course of atherosclerosis or restenosis.
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Ikeda et al. (1998) studied this question.
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