Implicações farmacogenéticas de polimorfismos da eNOS para drogas de ação cardiovascular

Silva, Pâmela Souza; Lacchini, Riccardo; Gomes, Valéria de Aguiar; Tanus‐Santos, José Eduardo

doi:10.1590/s0066-782x2011000200017

Cited by 18 publications

(18 citation statements)

References 66 publications

(85 reference statements)

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“…Studies have shown that fluvastatin and atorvastatin can increase the transcriptional activity of the eNOS gene. Statins can also inhibit the replication protein A1 (RPA1), a repressor of the transcriptional activity of eNOS (1,16,41), particularly in subjects with the CC genotype (1,12,38,91). This has been demonstrated by increased circulating levels of nitric oxide biomarkers (nitrite and nitrate) following administration of statins, regardless of the genotype, but being higher in C-allele carriers (1,12,16,41,82,83).…”

Section: Statinsmentioning

confidence: 99%

“…Statins can also increase eNOS expression and activitycompensating the genetic disadvantage of subjects with the CC genotype for the T786C polymorphism - (1,10,16,41,(94)(95)(96)(97)(98), effect on eNOS expression not being lowered when LDL cholesterol values normalized (94).…”

Section: Statinsmentioning

confidence: 99%

“…Correlations between eNOS gene polymorphisms and differentiated responses to cardiovascular drugs have also been reported (41). In this review we discuss the pharmacogenetic impact of eNOS polymorphisms on drugs that affect eNOS activity, such as antihypertensive drugs with a role in NO bioavailability.…”

mentioning

confidence: 91%

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Pharmacogenetic Implications of eNOS Polymorphisms (Glu298Asp, T786C, 4b/4a) in Cardiovascular Drug Therapy

Cozma

Fodor

Orășan

et al. 2019

In Vivo

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Endothelial nitric oxide synthase (NOS3 or eNOS) is the enzyme responsible for the highest production of nitric oxide, with the greatest impact on the cardiovascular system, encoded by the eNOS gene, which presents various polymorphisms. ENOS gene polymorphisms play an important role in the response to drugs affecting nitric oxide (NO) signaling. This review discusses the pharmacogenetic impact of eNOS polymorphisms on the response to drugs affecting NO activity: angiotensin converting enzyme inhibitors, angiotensin II receptor antagonists, calcium blockers, beta-blockers, diuretics, phosphodiesterase inhibitors, and statins. The identification of biomarkers that accurately predict particular phenotypes is a challenge that needs additional large studies, in different populations. Efforts should be oriented towards a more accurate evaluation of the effects of eNOS genetic variants on biochemical parameters reflecting eNOS gene expression and enzymatic activity, in different diseases, as well as following drug treatment. This approach will allow for a better understanding of the role of eNOS genetic variants in cardiovascular disease progression and for cardiovascular drug therapy optimization.

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Section: Statinsmentioning

confidence: 99%

Section: Statinsmentioning

confidence: 99%

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Pharmacogenetic Implications of eNOS Polymorphisms (Glu298Asp, T786C, 4b/4a) in Cardiovascular Drug Therapy

Cozma

Fodor

Orășan

et al. 2019

In Vivo

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“…Several polymorphisms have been associated with pre-eclampsia and other cardiovascular and hypertensive disorders 96–98. A relationship between eNOS polymorphisms and differential responses to several classes of cardiovascular drugs has been shown,99 some of which are used for the treatment of pre-eclampsia.…”

Section: Treatment and Prevention Of Pre-eclampsiamentioning

confidence: 99%

The role of genetics in pre-eclampsia and potential pharmacogenomic interventions

Williams¹

2012

PGPM

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The pregnancy-specific condition pre-eclampsia not only affects the health of mother and baby during pregnancy but also has long-term consequences, increasing the chances of cardiovascular disease in later life. It is accepted that pre-eclampsia has a placental origin, but the pathogenic mechanisms leading to the systemic endothelial dysfunction characteristic of the disorder remain to be determined. In this review we discuss some key factors regarded as important in the development of pre-eclampsia, including immune maladaptation, inadequate placentation, oxidative stress, and thrombosis. Genetic factors influence all of these proposed pathophysiological mechanisms. The inherited nature of pre-eclampsia has been known for many years, and extensive genetic studies have been undertaken in this area. Genetic research offers an attractive strategy for studying the pathogenesis of pre-eclampsia as it avoids the ethical and practical difficulties of conducting basic science research during the preclinical phase of pre-eclampsia when the underlying pathological changes occur. Although pharmacogenomic studies have not yet been conducted in pre-eclampsia, a number of studies investigating treatment for essential hypertension are of relevance to therapies used in pre-eclampsia. The pharmacogenomics of antiplatelet agents, alpha and beta blockers, calcium channel blockers, and magnesium sulfate are discussed in relation to the treatment and prevention of pre-eclampsia. Pharmacogenomics offers the prospect of individualized patient treatment, ensuring swift introduction of optimal treatment whilst minimizing the use of inappropriate or ineffective drugs, thereby reducing the risk of harmful effects to both mother and baby.

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“…NO is produced by NO-synthases (NOS), which catalyze the conversion of L-arginine to L-citrulline and NO. There are three isoforms of NOS: neuronal (nNOS), induced (iNOS) and endothelial (eNOS) [7]. It has been reported that eNOS is the predominant isoform of NOS expressed in normal adult bone.…”

Section: Introductionmentioning

confidence: 99%

The Association of eNOS Gene Polymorphism with Avascular Necrosis of Femoral Head

Zheng

Wang

et al. 2014

PLoS ONE

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ObjectivesNecrosis of femoral head is a severe pathological state with multiple etiologies. This study investigated the association of the 27-bp repeat polymorphism in intron 4 and G894T polymorphism in exon 7 of the endothelial nitric oxide synthase (eNOS) gene with the pathogenesis of avascular necrosis of femoral head (ANFH).MethodsA total of 125 non-traumatic ANFH patients and 126 healthy controls were recruited for this study. The 27-bp repeat polymorphisms in intron 4 were analyzed by polymerase chain reaction (PCR) and sequencing. The G894T polymorphisms in exon 7 were analyzed by PCR– restriction fragment length polymorphism (PCR-RFLP) analysis.ResultsAll alleles were observed in non-traumatic ANFH patients and control subjects. Both ANFH patients and idiopathic subgroup of ANFH patients showed higher frequency of the 4a/b genotype than controls (p = 0.001 and p = 0.020, respectively). Significantly higher frequency of G/T genotype was observed in ANFH patients and idiopathic subgroup of ANFH patients compared to controls (p = 0.009 and p = 0.035, respectively).ConclusioneNOS gene polymorphisms may be a risk factor for ANFH. The 27-bp repeat polymorphism in intron 4, G894T polymorphism in exon 7, and subsequently reduced eNOS activity may be involved in the etiology of idiopathic ANFH.

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Implicações farmacogenéticas de polimorfismos da eNOS para drogas de ação cardiovascular

Cited by 18 publications

References 66 publications

Pharmacogenetic Implications of eNOS Polymorphisms (Glu298Asp, T786C, 4b/4a) in Cardiovascular Drug Therapy

Pharmacogenetic Implications of eNOS Polymorphisms (Glu298Asp, T786C, 4b/4a) in Cardiovascular Drug Therapy

The role of genetics in pre-eclampsia and potential pharmacogenomic interventions

The Association of eNOS Gene Polymorphism with Avascular Necrosis of Femoral Head

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