Association of left ventricular mass with the AGTR1 A1166C polymorphism

Jin, Yu; Kuznetsova, Tatiana; Thijs, Lutgarde; Schmitz, Boris; Liu, Yan-Ping; Asayama, Kei; Brand, Stefan-Martin; Heymans, Stéphane; Brand, Eva; Fagard, Robert; Staessen, Jan A.

doi:10.1038/ajh.2011.244

Cited by 23 publications

(23 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In the present study, we have found increased septal and anterior wall thickness in uremic animals. Additionally, plasma ANG II level, which is an indirect marker of hypertension and left ventricular hypertrophy (20,27,28,43,58), was also higher in uremic rats. These results together with literature data (1,33,38,41) suggest the development of a minimal left ventricular hypertrophy in uremic animals at week 30 in our present study.…”

Section: Discussionmentioning

confidence: 97%

“…Immediately after excision of the heart, blood was collected from the thoracic cavity to measure plasma uric acid, carbamide, and creatinine levels to verify the development of uremia. Some plasma was used for the determination of ANG II as an indirect marker of hypertension and hypertrophy (20,27,28,43,58) and nitrotyrosine as a marker of systemic nitrosative stress (7). To assess the cardioprotective effect of ischemic preconditioning in the hearts of uremic and sham-operated animals, the perfused hearts were subjected to ischemia/reperfusion with or without preconditioning protocol.…”

Section: This Investigation Conforms To the National Institutes Of Hementioning

confidence: 99%

See 1 more Smart Citation

Preconditioning protects the heart in a prolonged uremic condition

Kocsis

Sárközy

Bencsik

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

Metabolic diseases such as hyperlipidemia and diabetes attenuate the cardioprotective effect of ischemic preconditioning. In the present study, we examined whether another metabolic disease, prolonged uremia, affects ischemia/reperfusion injury and cardioprotection by ischemic preconditioning. Uremia was induced by partial nephrectomy in male Wistar rats. The development of uremia was verified 29 wk after surgery. Transthoracic echocardiography was performed to monitor cardiac function. At week 30, hearts of nephrectomized and sham-operated rats were isolated and subjected to a 30-min coronary occlusion followed by 120 min reperfusion with or without preceding preconditioning induced by three intermittent cycles of brief ischemia and reperfusion. In nephrectomized rats, plasma uric acid, carbamide, and creatinine as well as urine protein levels were increased as compared with shamoperated controls. Systolic anterior and septal wall thicknesses were increased in nephrectomized rats, suggesting the development of a minimal cardiac hypertrophy. Ejection fraction was decreased and isovolumic relaxation time was shortened in nephrectomized rats demonstrating a mild systolic and diastolic dysfunction. Infarct size was not affected significantly by nephrectomy itself. Ischemic preconditioning significantly decreased infarct size from 24.8 Ϯ 5.2% to 6.6 Ϯ 1.3% in the sham-operated group and also in the uremic group from 35.4 Ϯ 9.5% to 11.9 Ϯ 3.1% of the area at risk. Plasma ANG II and nitrotyrosine were significantly increased in the uremic rats. We conclude that although prolonged experimental uremia leads to severe metabolic changes and the development of a mild myocardial dysfunction, the cardioprotective effect of ischemic preconditioning is still preserved. chronic renal failure; myocardium; ischemic preconditioning; infarct size; myocardial function ISCHEMIC PRECONDITIONING IS a well-characterized endogenous adaptive response of the myocardium in which brief cycles of ischemia markedly enhance the ability of the heart to withstand a subsequent ischemic injury (15). Although preconditioning confers remarkable cardioprotection in a variety of species (15, 44), including humans (21, 49, 55), we and others have shown that its effectiveness is attenuated by some risk factors and comorbidities such as metabolic diseases including hyperlipidemia (14 -16) and diabetes (35, 54) both in animal models and humans (15).

show abstract

Section: Discussionmentioning

confidence: 97%

Section: This Investigation Conforms To the National Institutes Of Hementioning

confidence: 99%

Preconditioning protects the heart in a prolonged uremic condition

Kocsis

Sárközy

Bencsik

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

show abstract

“…Вместе с тем, результаты многоцентровых исследований по ассо-циации SNP А1166С гена AGT2R1 с риском развития БСК для разных этнических групп противоречивы и неоднозначны. Единичные работы в России не отражают генетического разнообразия в распреде-лении 1166С полиморфизмов гена AGT2R1 и их ассо-циаций с ССЗ [8][9][10][11][12][13][14][15].…”

Section: Discussionunclassified

“…С1166С генотип и 1166С аллель ассоциированы с повышенным риском развития сердечно-сосудис-тых заболеваний и, в частности, коронарного атеро-склероза [9,10,12,14,15].…”

Section: литератураunclassified

Prognostic Role of A1166c Polymorphisms of the Angiotensine Ii Receptor Gene (Agt2r1) in Coronary Atherosclerosis Among Adyghea Republic Inhabitants

Ашканова¹,

Муженя²,

Пшидаток³

et al. 2015

Ross. kardiol. ž.

View full text Add to dashboard Cite

Цель. Исследование ассоциации A1166/166C полиморфизмов гена сосудис-того рецептора 1 типа ангиотензина II (AGT2R1) с развитием коронарного и периферического атеросклероза в этнических группах населения Респу-блики Адыгея. Материал и методы. Распределение A1166/166C полиморфных вариантов гена AGT2R1 исследовано "single nucleotide polymorphism" (SNP) -методом с аллель-специфическими праймерами и электрофоретической детекцией результатов (НПФ "Литех"). Полиморфизмы гена AGT2R1 (rs5186) с нуклео-тидной заменой аденина на цитозин (А>C) в 1166 позиции гена AGT2R1 типи-рованы в образцах геномной ДНК доноров (n=143) и больных с сердечно-сосу-дистыми заболеваниями (n=39) в возрасте 23-65 лет из двух этнических групп -адыгов и русских. Экспериментальные данные проанализированы адекватными статистическими методами SPSS Statistics 17.0. Результаты. В группе больных с осложнениями коронарного и перифериче-ского атеросклероза выявлено статистически значимое повышение частоты мутантной 1166С аллели и патологического гомозиготного генотипа С1166С. Риск развития сердечно-сосудистых заболеваний у носителей 1166С аллеля возрастает в 3,77 раз (c 2 =26,07; р=0,00003), а в случае с гомозиготным "мутантным" СС генотипом -в 10,36 раз (c 2 =31,20; р=0,00002), что позволяет использовать 1166C аллель и С1166С генотип AGT2R1 в качестве генетических предикторов коронарного атеросклероза и маркеров донозологической диа-гностики ишемической болезни сердца (c 2 =42,96; р=0,0000005; OR (95%)=17,37). Заключение. Полученные экспериментальные данные в сочетании с допол-нительными инструментальными исследованиями функционального состоя-ния сердечно-сосудистой системы, будут способствовать улучшению точно-сти диагностики атеросклероза и возможных осложнений последнего на ран-них этапах, что позволит снизить инвалидизацию и смертность среди лиц трудоспособного возраста. Aim. The investigation of A1166/166C polymorphisms of the vascular receptor 1 type of angiotensine II gene (AGT2R1) association with the development of coronary and peripheral atherosclerosis in ethnic groups of Adyghea Republic inhabitants. Material and methods. The spread of A1166/166C polymorphic variants of the gene AGT2R1 was studied via the "single nucleotide polymorphism" (SNP) -method with allele-specific primers and electrophoretic results detection (by SPF "Litech"). Gene polymorphisms AGT2R1 (rs5186) with nucleotide replacement of adenine by cytosine (А>C) in the 1166th position of gene AGT2R1 were typified in the samples of donors genomic DNA (n=143) and of those with cardiovascular diseases (n=39) at the age 23-65 y. o. from two ethnic subgroups -Adyghes and Russians. The data was processed via software SPSS Statistics 17.0. Results. In the group of those with complicated coronary and peripheral atherosclerosis there was statistically significant increase of the prevalence of mutant 1166C allele and of pathological monozygous genotype C1166C. The risk of cardiovascular diseases in the carriers of 1166C allele increases 3,77 times (c 2 =26,07; р=0,00003), and in the case ...

show abstract

“…A recent study showed a miR signature in plasma of patients with essential hypertension, which differed from their healthy counterparts: 27 miRs were differentially expressed. 9 The evidence for the interplay among miR-155, the angiotensin receptor 1, A1166C polymorphism, and angiotensin receptor 1 protein expression levels 10,11 provides a possible pathogenetic role for a miR in cardiac hypertrophy, whereas the description of a genetic variant in the 3′ untranslated region of vacuolar H+ ATPase ATPV0A1 creates a miR-637-binding motif related to hypertension risk by interfering with the fine-tuning of several vasoactive substances, including chromogranin A as precursor of catestatin, an inhibitor of catecholamine release. 12 A refreshing point of view would be to study the effect of antihypertensive medication on miR profiles.…”

Section: Are Mirs Of Pathogenetic Importance In Arterial Hypertensionmentioning

confidence: 99%

MicroRNAs Are Involved in End-Organ Damage During Hypertension

Heggermont

Heymans

2012

Hypertension

View full text Add to dashboard Cite

Even in the new millennium, arterial hypertension remains a serious condition, with considerable morbidity and mortality worldwide. Crucial in managing the disease is not only lowering arterial blood pressure but also preventing or treating the typical end-organ damage caused by long-lasting and inadequately treated hypertension. In the past decade, it has been shown that microRNAs (miRs) are involved in several hypertension-related pathologies, such as cardiac hypertrophy and fibrosis, hypertensive heart failure, renal fibrosis, kidney failure, and, to a lesser extent, eye disease and hemorrhagic stroke. Whereas others extensively reviewed the role of miRs in atherosclerosis and vascular disease, this review focuses on their role in target organ damage during arterial hypertension. We emphasize the involvement of miRs in pathological end-organ remodeling processes and try to demonstrate some common miR signatures in distinct end organs. Hence, we aimed to provide proof of arterial hypertension being a systemic disease, similar to diabetes mellitus or metabolic syndrome. Furthermore, miRs that act on one particular process in different end organs are interesting therapeutic targets. Some future perspectives in miR research are highlighted with respect to novel therapeutic strategies in the cardiovascular field.

show abstract

Association of left ventricular mass with the AGTR1 A1166C polymorphism

Abstract: LV mass index is associated with the AGTR1 A1166C polymorphism. Further research should clarify to what extent this association might be mediated via different expression of AGTR1 as modulated by microRNA-155.

Cited by 23 publications

References 40 publications

Preconditioning protects the heart in a prolonged uremic condition

Preconditioning protects the heart in a prolonged uremic condition

Prognostic Role of A1166c Polymorphisms of the Angiotensine Ii Receptor Gene (Agt2r1) in Coronary Atherosclerosis Among Adyghea Republic Inhabitants

MicroRNAs Are Involved in End-Organ Damage During Hypertension

Contact Info

Product

Resources

About