Related Experiment Video
Updated: Apr 25, 2026

Application of Genetically Encoded Fluorescent Nitric Oxide (NO•) Probes, the geNOps, for Real-time Imaging of NO• Signals in Single Cells
Published on: March 16, 2017
Genetics of NO Deficiency
Kirsten Leineweber1, Sven Moosmang2, Dan Paulson3
1Bayer AG, Disease Genomics, Wuppertal, Germany.
Insights
Nitric oxide-cyclic guanosine monophosphate (NO-cGMP) pathway gene variants can lead to NO-cGMP deficiency, impacting cardiovascular disease risk. This review explores the role of NO-cGMP deficiency in cardiovascular health.
Area of Science:
- Cardiovascular Physiology
- Molecular Biology
- Genetics
Background:
- The nitric oxide-cyclic guanosine monophosphate (NO-cGMP) pathway is crucial for cardiovascular homeostasis.
- Genetic variations impacting this pathway can lead to NO-cGMP deficiency, potentially influencing cardiovascular disease (CVD).
- NO-cGMP deficiency arises from various mechanisms, including issues with nitric oxide synthase (NOS) and altered cGMP metabolism.
Purpose of the Study:
- To review the evidence linking NO-cGMP pathway deficiency to cardiovascular disease.
- To discuss the role of genetic variants, polymorphisms, haplotypes, and racial disparities in NO-cGMP deficiency and CVD.
- To examine key components of the NO-cGMP pathway implicated in cardiovascular health.
Main Methods:
- Literature review of genetic association studies.
- Analysis of evidence linking NO-cGMP pathway dysfunction to cardiovascular outcomes.
- Discussion of specific NO-cGMP pathway components and their roles.
Main Results:
- Genetic variants in NO-cGMP pathway genes are associated with cardiovascular disease prevalence and progression.
- Multiple factors contribute to NO-cGMP deficiency, affecting nitric oxide bioavailability and cGMP signaling.
- Evidence supports a significant role for NO-cGMP pathway dysfunction in various cardiovascular conditions.
Conclusions:
- NO-cGMP pathway deficiency, influenced by genetic factors, is a significant contributor to cardiovascular disease.
- Understanding these genetic links and pathway components is vital for cardiovascular research and potential therapeutic strategies.
- Further investigation into genetic disparities and NO-cGMP pathway modulation is warranted for CVD prevention and treatment.
Abstract:
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.
More Related Videos
Related Concept Videos
Overview of Nitrogen Metabolism
The largest pool of nitrogen available in the terrestrial ecosystem is gaseous nitrogen (N2) from the air, but this...
Nitric Oxide Signaling Pathway
Antihypertensive Drugs: Vasodilators
Antianginal Drugs: Nitrates and β-Blockers
Organic nitrates, such as nitroglycerin, play a pivotal role. Once metabolized, they liberate nitric oxide, a molecular marvel. Nitric oxide triggers guanylyl cyclase and augments cGMP production. This biochemical cascade orchestrates the relaxation of vascular smooth muscles, ushering in vasodilation and enhancing coronary blood flow....
Human Genetics
The complex relationship between genetics and psychology is observable through common biological components such...
Coronary Artery Disease II: Pathophysiology

