Glu298Asp polymorphism of the eNOS gene is associated with coronary collateral development

Güleç, Sadi; Karabulut, Halil Gürhan; Ongun, Aydan; Ozdol, Cagdas; Turhan, Sibel; Altın, Timuçin; Tutar, Eralp; Genç, Yasemin; Erol, Çetin

doi:10.1016/j.atherosclerosis.2007.09.037

Cited by 23 publications

(24 citation statements)

References 33 publications

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“…Consistently, a recent study performed on 60 Indian patients with documented history of CAD reported a significantly higher frequency of rs1799983 ( p < 0.05) compared to control subjects, indicating that variations in NOS3 gene may be useful clinical markers of endothelial dysfunction in CAD [54]. Interestingly, another association between rs1799983_GT and impaired collateral development has been observed in patients with a high-grade coronary stenosis or occlusion [19]. …”

Section: Discussionmentioning

confidence: 57%

Role of genetic polymorphisms of ion channels in the pathophysiology of coronary microvascular dysfunction and ischemic heart disease

et al. 2013

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Conventionally, ischemic heart disease (IHD) is equated with large vessel coronary disease. However, recent evidence has suggested a role of compromised microvascular regulation in the etiology of IHD. Because regulation of coronary blood flow likely involves activity of specific ion channels, and key factors involved in endothelium-dependent dilation, we proposed that genetic anomalies of ion channels or specific endothelial regulators may underlie coronary microvascular disease. We aimed to evaluate the clinical impact of single-nucleotide polymorphisms in genes encoding for ion channels expressed in the coronary vasculature and the possible correlation with IHD resulting from microvascular dysfunction. 242 consecutive patients who were candidates for coronary angiography were enrolled. A prospective, observational, single-center study was conducted, analyzing genetic polymorphisms relative to (1) NOS3 encoding for endothelial nitric oxide synthase (eNOS); (2) ATP2A2 encoding for the Ca2+/H+-ATPase pump (SERCA); (3) SCN5A encoding for the voltage-dependent Na+ channel (Nav1.5); (4) KCNJ8 and KCNJ11 encoding for the Kir6.1 and Kir6.2 subunits of K-ATP channels, respectively; and (5) KCN5A encoding for the voltage-gated K+ channel (Kv1.5). No significant associations between clinical IHD manifestations and polymorphisms for SERCA, Kir6.1, and Kv1.5 were observed (p > 0.05), whereas specific polymorphisms detected in eNOS, as well as in Kir6.2 and Nav1.5 were found to be correlated with IHD and microvascular dysfunction. Interestingly, genetic polymorphisms for ion channels seem to have an important clinical impact influencing the susceptibility for microvascular dysfunction and IHD, independent of the presence of classic cardiovascular risk factors.

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Section: Discussionmentioning

confidence: 57%

Role of genetic polymorphisms of ion channels in the pathophysiology of coronary microvascular dysfunction and ischemic heart disease

et al. 2013

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“…EDNO maintains arterial endothelial cell integrity and promotes endothelial cell migration [39], regulates both in-vitro and in-vivo angiogenesis [40,41], plays fundamental role in the acute modulation of collateral circuit vasomotor tone such that NO-mediated increases in vascular conductance allows for greater collateral dependent blood-flow to the distal hindlimb [42]. EDNO is implicated in the vascular remodeling of preexisting arterioles to highcapacity collateral conduits [43,44], has a pivotal role in the collateral-enhancing effect of vascular endothelial growth factor [45] whereas endothelial nitric oxide synthase Asp298 allele was reported to be associated with poor collateral development [46].…”

Section: Discussionmentioning

confidence: 98%

Association of paraoxonase activity and coronary collateral flow

Yıldız¹,

Sezen²,

Gür³

et al. 2008

Coronary Artery Disease

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“…37 Endothelial NOS gene Glu298Asp polymorphism was also found to be related with poor coronary collateral development, indicating the importance of NO in collateral formation. 19 Previous studies showed that there is a negative relationship between collateral development and cardiovascular risk factors related with endothelial dysfunction such as DM, metabolic syndrome, and obesity. 42–45 Angiotensin-converting enzyme gene polymorphism has negative effects on endothelial function.…”

Section: Discussionmentioning

confidence: 99%

Angiotensin-Converting Enzyme DD Polymorphism is Associated with Poor Coronary Collateral Circulation in Patients with Coronary Artery Disease

Ceyhan

Kadı

Çelik

et al. 2012

Journal of Investigative Medicine

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Glu298Asp polymorphism of the eNOS gene is associated with coronary collateral development

Cited by 23 publications

References 33 publications

Role of genetic polymorphisms of ion channels in the pathophysiology of coronary microvascular dysfunction and ischemic heart disease

Role of genetic polymorphisms of ion channels in the pathophysiology of coronary microvascular dysfunction and ischemic heart disease

Association of paraoxonase activity and coronary collateral flow

Angiotensin-Converting Enzyme DD Polymorphism is Associated with Poor Coronary Collateral Circulation in Patients with Coronary Artery Disease

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