Role of sGC-dependent NO signalling and myocardial infarction risk

Jana Wobst; Thorsten Kessler; Tan An Dang; Jeanette Erdmann; Heribert Schunkert

doi:10.1007/s00109-015-1265-3

Role of sGC-dependent NO signalling and myocardial infarction risk

Jana Wobst, Thorsten Kessler, Tan An Dang, Jeanette Erdmann, Heribert Schunkert^*

^*Corresponding author for this work

Technical University of Munich

26 Citations (Scopus)

Abstract

The NO/cGMP pathway plays an important role in many physiological functions and pathophysiological conditions. In the last few years, several genetic and functional studies pointed to an underestimated role of this pathway in the development of atherosclerosis. Indeed, several genetic variants of key enzymes modulating the generation of NO and cGMP have been strongly associated with coronary artery disease and myocardial infarction risk. In this review, we aim to place the genomic findings on components of the NO/cGMP pathway, namely endothelial nitric oxide synthase, soluble guanylyl cyclase and phosphodiesterase 5A, in context of preventive and therapeutic strategies for treating atherosclerosis and its sequelae.

Original language	English
Journal	Journal of Molecular Medicine
Volume	93
Issue number	4
Pages (from-to)	383-394
Number of pages	12
ISSN	0946-2716
DOIs	https://doi.org/10.1007/s00109-015-1265-3
Publication status	Published - 20.03.2015

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abstract = "The NO/cGMP pathway plays an important role in many physiological functions and pathophysiological conditions. In the last few years, several genetic and functional studies pointed to an underestimated role of this pathway in the development of atherosclerosis. Indeed, several genetic variants of key enzymes modulating the generation of NO and cGMP have been strongly associated with coronary artery disease and myocardial infarction risk. In this review, we aim to place the genomic findings on components of the NO/cGMP pathway, namely endothelial nitric oxide synthase, soluble guanylyl cyclase and phosphodiesterase 5A, in context of preventive and therapeutic strategies for treating atherosclerosis and its sequelae.",

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T1 - Role of sGC-dependent NO signalling and myocardial infarction risk

AU - Wobst, Jana

AU - Kessler, Thorsten

AU - Dang, Tan An

AU - Erdmann, Jeanette

AU - Schunkert, Heribert

PY - 2015/3/20

Y1 - 2015/3/20

N2 - The NO/cGMP pathway plays an important role in many physiological functions and pathophysiological conditions. In the last few years, several genetic and functional studies pointed to an underestimated role of this pathway in the development of atherosclerosis. Indeed, several genetic variants of key enzymes modulating the generation of NO and cGMP have been strongly associated with coronary artery disease and myocardial infarction risk. In this review, we aim to place the genomic findings on components of the NO/cGMP pathway, namely endothelial nitric oxide synthase, soluble guanylyl cyclase and phosphodiesterase 5A, in context of preventive and therapeutic strategies for treating atherosclerosis and its sequelae.

AB - The NO/cGMP pathway plays an important role in many physiological functions and pathophysiological conditions. In the last few years, several genetic and functional studies pointed to an underestimated role of this pathway in the development of atherosclerosis. Indeed, several genetic variants of key enzymes modulating the generation of NO and cGMP have been strongly associated with coronary artery disease and myocardial infarction risk. In this review, we aim to place the genomic findings on components of the NO/cGMP pathway, namely endothelial nitric oxide synthase, soluble guanylyl cyclase and phosphodiesterase 5A, in context of preventive and therapeutic strategies for treating atherosclerosis and its sequelae.

UR - https://www.scopus.com/pages/publications/84925504575

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DO - 10.1007/s00109-015-1265-3

M3 - Scientific review articles

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SN - 0946-2716

VL - 93

SP - 383

EP - 394

JO - Journal of Molecular Medicine

JF - Journal of Molecular Medicine

IS - 4

ER -

Role of sGC-dependent NO signalling and myocardial infarction risk

Abstract

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