Journal
NITRIC OXIDE-BIOLOGY AND CHEMISTRY
Volume 76, Issue -, Pages 105-112Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.niox.2018.03.019
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Funding
- Deutsche Forschungsgemeinschaft (DFG) [Sonderforschungsbereich CRC 1123]
- Corona-Stiftung as part of the Junior Research Group Translational Cardiovascular Genomics
- Fondation Leducq [12CVD02]
- German Federal Ministry of Education and Research (BMBF) [JTC2017_21-040, 01ZX1706C, 01ZX1313A-2014]
- European Union [HEALTH-F2-2013-601456]
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In the past ten years, several chromosomal loci have been identified by genome-wide association studies to influence the risk of coronary artery disease (CAD) and its risk factors. The GUCY1A3 gene encoding the alpha(1) subunit of the soluble guanylyl cyclase (sGC) resides at one of these loci and has been strongly associated with blood pressure and CAD risk. More recently, further genes in the pathway encoding the endothelial nitric oxide synthase, the phosphodiesterases 3A and 5A, and the inositol 1,4,5-trisphosphate receptor I-associated protein (IRAG), i.e., NOS3, PDE3A, PDE5A, and MRVI1, respectively, were likewise identified as CAD risk genes. In this review, we highlight the genetic findings linking variants in NO-cGMP signaling and cardiovascular disease, discuss the potential underlying mechanisms which might propagate the development of atherosclerosis, and speculate about therapeutic implications.
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