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JOURNAL ARTICLE
REVIEW
Genetics of NO Deficiency.
American Journal of Cardiology 2017 October 16
The nitric oxide-cyclic guanosine monophosphate (NO-cGMP) pathway plays a key role in regulating cardiovascular homeostasis, and genetic variants allocated to NO-cGMP pathway genes, leading to NO-cGMP deficiency, may influence the prevalence or course of cardiovascular disease. NO-cGMP deficiency can be caused by nitric oxide synthase substrate deficiency, substrate competition, defects, or uncoupling; endogenous inhibitors of nitric oxide synthase; decreased cGMP production; or increased cGMP degradation. This review presents evidence supporting the role of NO-cGMP deficiency in cardiovascular disease, including findings from genetic association studies for particular polymorphisms, haplotypes, and racial disparities. NO-cGMP pathway components including arginases, guanosine-5'-triphosphate cyclohydrolase 1, nitric oxide synthase, dimethylarginine dimethylaminohydrolases, soluble guanylyl cyclase, protein kinase G, phosphodiesterase 5, and natriuretic peptides will be discussed.
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