Nitric oxide synthase Glu298Asp gene polymorphism in cardiovascular diseases

Ischemic heart disease (IHD), the leading cause of death worldwide, is a multifactorial disease arising from the complex interplay of genetic and environmental factors. There is considerable evidence that nitric oxide (NO) plays an important role in protecting against atherosclerosis, the process...

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Main Authors:	Ibrahim, Wisam Nabeel, A.Talib, Norlelawati, Abdullah, Nor Zamzila
Format:	Conference or Workshop Item
Language:	English English
Published:	2014
Subjects:	QP Physiology
Online Access:	http://irep.iium.edu.my/41518/ http://irep.iium.edu.my/41518/2/nitric_oxide.pdf http://irep.iium.edu.my/41518/5/90.pdf

id	iium-41518
recordtype	eprints
spelling	iium-415182018-05-05T17:52:14Z http://irep.iium.edu.my/41518/ Nitric oxide synthase Glu298Asp gene polymorphism in cardiovascular diseases Ibrahim, Wisam Nabeel A.Talib, Norlelawati Abdullah, Nor Zamzila QP Physiology Ischemic heart disease (IHD), the leading cause of death worldwide, is a multifactorial disease arising from the complex interplay of genetic and environmental factors. There is considerable evidence that nitric oxide (NO) plays an important role in protecting against atherosclerosis, the process underlying IHD ( Spence et al., 2004). Endothelial-derived nitric oxide (NO) is synthesized by nitric oxide synthase (NOS). Variations in the human NOS gene have been identified. A single base nucleotide exchange polymorphism within exon 7 (G to T transition) at position 894 results in an exchange of glutamate (Glu) for an aspartate (Asp) amino acid, respectively, at position 298 in the enzyme (Hingorani ,1998). NOS Asp298 is subjected to selective proteolytic cleavage in endothelial cells and vascular tissues that might account for reduced vascular NO generation (Akhter, Biswas, & Saxena, 2009). Decreased NO and oxidative excess may activate matrix metalloproteinase (MMP) which weaken the fibrous cap. Because NO inhibits platelet aggregation, reduced NO contributes to thrombogenicity. Thus, endothelial dysfunction with reduced NO bioavailability, increased oxidant excess, and expression of adhesion molecules contributes not only to initiation but also to progression of atherosclerotic plaque formation and triggering of cardiovascular events such as ischemic heart disease(Uemura,2001). 2014-06-10 Conference or Workshop Item NonPeerReviewed application/pdf en http://irep.iium.edu.my/41518/2/nitric_oxide.pdf application/pdf en http://irep.iium.edu.my/41518/5/90.pdf Ibrahim, Wisam Nabeel and A.Talib, Norlelawati and Abdullah, Nor Zamzila (2014) Nitric oxide synthase Glu298Asp gene polymorphism in cardiovascular diseases. In: International Research, Invention and Innovation Exhibition 2014 (IRIIE2014), 11th -13th June 2014, Cultural Activity Center (CAC), Internatioanal Islamic University Malaysia. (Unpublished)
repository_type	Digital Repository
institution_category	Local University
institution	International Islamic University Malaysia
building	IIUM Repository
collection	Online Access
language	English English
topic	QP Physiology
spellingShingle	QP Physiology Ibrahim, Wisam Nabeel A.Talib, Norlelawati Abdullah, Nor Zamzila Nitric oxide synthase Glu298Asp gene polymorphism in cardiovascular diseases
description	Ischemic heart disease (IHD), the leading cause of death worldwide, is a multifactorial disease arising from the complex interplay of genetic and environmental factors. There is considerable evidence that nitric oxide (NO) plays an important role in protecting against atherosclerosis, the process underlying IHD ( Spence et al., 2004). Endothelial-derived nitric oxide (NO) is synthesized by nitric oxide synthase (NOS). Variations in the human NOS gene have been identified. A single base nucleotide exchange polymorphism within exon 7 (G to T transition) at position 894 results in an exchange of glutamate (Glu) for an aspartate (Asp) amino acid, respectively, at position 298 in the enzyme (Hingorani ,1998). NOS Asp298 is subjected to selective proteolytic cleavage in endothelial cells and vascular tissues that might account for reduced vascular NO generation (Akhter, Biswas, & Saxena, 2009). Decreased NO and oxidative excess may activate matrix metalloproteinase (MMP) which weaken the fibrous cap. Because NO inhibits platelet aggregation, reduced NO contributes to thrombogenicity. Thus, endothelial dysfunction with reduced NO bioavailability, increased oxidant excess, and expression of adhesion molecules contributes not only to initiation but also to progression of atherosclerotic plaque formation and triggering of cardiovascular events such as ischemic heart disease(Uemura,2001).
format	Conference or Workshop Item
author	Ibrahim, Wisam Nabeel A.Talib, Norlelawati Abdullah, Nor Zamzila
author_facet	Ibrahim, Wisam Nabeel A.Talib, Norlelawati Abdullah, Nor Zamzila
author_sort	Ibrahim, Wisam Nabeel
title	Nitric oxide synthase Glu298Asp gene polymorphism in cardiovascular diseases
title_short	Nitric oxide synthase Glu298Asp gene polymorphism in cardiovascular diseases
title_full	Nitric oxide synthase Glu298Asp gene polymorphism in cardiovascular diseases
title_fullStr	Nitric oxide synthase Glu298Asp gene polymorphism in cardiovascular diseases
title_full_unstemmed	Nitric oxide synthase Glu298Asp gene polymorphism in cardiovascular diseases
title_sort	nitric oxide synthase glu298asp gene polymorphism in cardiovascular diseases
publishDate	2014
url	http://irep.iium.edu.my/41518/ http://irep.iium.edu.my/41518/2/nitric_oxide.pdf http://irep.iium.edu.my/41518/5/90.pdf
first_indexed	2023-09-18T20:59:27Z
last_indexed	2023-09-18T20:59:27Z
_version_	1777410524651192320

Nitric oxide synthase Glu298Asp gene polymorphism in cardiovascular diseases

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