Abstract
Vascular endothelial dysfunction is now recognized as a common phenomenon in an array of cardiovascular disorders. Production of nitric oxide via the endothelial isoform of nitric oxide synthase [eNOS (previously termed NOS3 or ecNOS)] is vital for a healthy endothelium; several polymorphic variations of the gene encoding eNOS (NOS3) are now known and have been investigated with respect to disease risk. Surprisingly, only approximately half of these studies have demonstrated significant associations between NOS3 polymorphisms and cardiovascular disease, and many reports are contradictory. Central issues include adequate statistical power, appropriateness of control cohorts, multigene interactions and plausible biological consequences. So far, the inconsistencies are not unique to the NOS3 polymorphisms, but probably represent the broad challenges in defining genetic aspects of complex disease processes.
Original language | English |
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Pages (from-to) | 361-368 |
Number of pages | 8 |
Journal | Trends in Pharmacological Sciences |
Volume | 22 |
Issue number | 7 |
DOIs | |
State | Published - Jul 1 2001 |
Bibliographical note
Funding Information:S.K.W. was supported by a graduate research fellowship from the Royal Thai Government. This work was supported in part by NIH grants HL59791, DK55053, HL63067 and NS34524.
ASJC Scopus subject areas
- Toxicology
- Pharmacology