Meta-analysis of association of ACE2 G8790A polymorphism with Chinese Han essential hypertension

Zhou, Jidong; Jy, Yang

doi:10.1177/1470320309103047

Cited by 17 publications

(16 citation statements)

References 9 publications

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“…The results of the current research conformed to those of Zhou and Yang (2009) who meta-analyzed the ACE2 G8790A gene polymorphism and EH in a Chinese Han population. The ACE2 G8790A gene polymorphism might not be a genetic risk factor for EH in the said population.…”

Section: Discussionsupporting

confidence: 86%

“…They found no significant association of ACE2 G8790A gene polymorphism and EH in the female Chinese population. Zhou and Yang (2009) performed a meta-analysis on the ACE2 G8790A polymorphism with Chinese Han EH and they concluded that ACE2 G8790A polymorphism might not be genetic risk factor for EH in a Chinese Han population. In contrast, Lu et al (2012) also conducted a similar meta-analysis and they found that ACE2 G8790A polymorphism was probably a genetic risk factor for EH across different ethnic populations in female subjects and in Han-Chinese male subjects.…”

Section: Introductionmentioning

confidence: 99%

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Lack of Association of ACE2 G8790A Gene Mutation with Essential Hypertension in the Chinese Population: A Meta-Analysis Involving 5260 Subjects

Li¹

2012

Front. Physio.

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Background: The angiotensin converting enzyme 2 (ACE2) G8790A gene polymorphism has been associated with the susceptibility to essential hypertension (EH), but the results are disputable. Objective and Methods: To investigate the relationship between the ACE2 G8790A gene polymorphism and EH, eight separate studies with 5260 subjects were meta-analyzed. The pooled odds ratio (OR) and its corresponding 95% confidence interval (CI) were calculated by a random effect model. Results: In the ACE2 G8790A gene polymorphism and EH meta-analysis in a Chinese population, no significant association was found between the ACE2 G8790A gene polymorphism and EH (OR: 1.03, 95% CI: 0.87–1.21, P = 0.76). In the stratified analysis by gender, no significant risk was found among males (OR: 1.06, 95% CI: 0.82–1.36, P = 0.66) or females (OR: 0.98, 95% CI: 0.77–1.24, P = 0.85). Under a dominant model of inheritance in the female subgroup, the pooled OR for the GG/GA + AA value was 1.01 (95% CI: 0.82–1.25, P = 0.92). Under a recessive model of inheritance in the female subgroup, the pooled OR for the AA/AG + GG value was 0.93 (95% CI: 0.50–1.73, P = 0.83). Conclusion: The current meta-analysis suggested that the ACE2 G8790A gene polymorphism might not be related to the increased EH risk in the Chinese population.

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Section: Discussionsupporting

confidence: 86%

Section: Introductionmentioning

confidence: 99%

Lack of Association of ACE2 G8790A Gene Mutation with Essential Hypertension in the Chinese Population: A Meta-Analysis Involving 5260 Subjects

Li¹

2012

Front. Physio.

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“…Two meta-analyses of the rs2285666 SNP have been reported with conflicting results (Zhou and Yang, 2009;Lu et al, 2012). One study had a combined total of 2528 Chinese Han subjects with hypertension and 2024 ethnicity matched normotensive controls and reported no association with hypertension (Zhou and Yang, 2009). The other study, a meta-analysis of 7251 hypertensive patients, reported a significant association between the rs2285666 AA genotype with hypertension in females only .…”

Section: Ace2 Gene Association Studies and Hypertensionmentioning

confidence: 99%

From gene to proteinâ€”experimental and clinical studies of ACE2 in blood pressure control and arterial hypertension

et al. 2014

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Hypertension is a major risk factor for stroke, coronary events, heart and renal failure, and the renin-angiotensin system (RAS) plays a major role in its pathogenesis. Within the RAS, angiotensin converting enzyme (ACE) converts angiotensin (Ang) I into the vasoconstrictor Ang II. An “alternate” arm of the RAS now exists in which ACE2 counterbalances the effects of the classic RAS through degradation of Ang II, and generation of the vasodilator Ang 1-7. ACE2 is highly expressed in the heart, blood vessels, and kidney. The catalytically active ectodomain of ACE2 undergoes shedding, resulting in ACE2 in the circulation. The ACE2 gene maps to a quantitative trait locus on the X chromosome in three strains of genetically hypertensive rats, suggesting that ACE2 may be a candidate gene for hypertension. It is hypothesized that disruption of tissue ACE/ACE2 balance results in changes in blood pressure, with increased ACE2 expression protecting against increased blood pressure, and ACE2 deficiency contributing to hypertension. Experimental hypertension studies have measured ACE2 in either the heart or kidney and/or plasma, and have reported that deletion or inhibition of ACE2 leads to hypertension, whilst enhancing ACE2 protects against the development of hypertension, hence increasing ACE2 may be a therapeutic option for the management of high blood pressure in man. There have been relatively few studies of ACE2, either at the gene or the circulating level in patients with hypertension. Plasma ACE2 activity is low in healthy subjects, but elevated in patients with cardiovascular risk factors or cardiovascular disease. Genetic studies have investigated ACE2 gene polymorphisms with either hypertension or blood pressure, and have produced largely inconsistent findings. This review discusses the evidence regarding ACE2 in experimental hypertension models and the association between circulating ACE2 activity and ACE2 polymorphisms with blood pressure and arterial hypertension in man.

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“…On the other hand, some reports found no association between ACE2 and hypertension (51;52) and ACE2 and a risk for sudden cardiac death in women or men (53) underlining the necessity for further evaluation of the impact of ACE2 gene variants on cardiovascular disease in human population.…”

Section: Ace2 and Cardiac Diseasementioning

confidence: 99%

ACE2: Angiotensin II/Angiotensin-(1–7) Balance in Cardiac and Renal Injury

et al. 2014

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Our current recognition of the renin-angiotensin system is more convoluted than originally thought due to the discovery of multiple novel enzymes, peptides, and receptors inherent to this interactive biochemical cascade. Over the last decade angiotensin converting enzyme 2 (ACE2) has emerged as a key player in the pathophysiology of hypertension and cardiovascular and renal disease due to its pivotal role in metabolizing vasoconstrictive/hypertrophic/proliferative angiotensin II into favorable angiotensin-(1-7). This review addresses a considerable advancement in research on the role of tissue ACE2 in development and progression of hypertension and cardiorenal injury. We also summarize the results from recent clinical and experimental studies suggesting that serum or urine soluble ACE2 may serve as a novel biomarker or independent risk factor relevant for diagnosis and prognosis of cardiorenal disease. Recent proceedings on novel therapeutic approaches to enhance ACE2/angiotensin-(1-7) axis are also reviewed.

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Meta-analysis of association of ACE2 G8790A polymorphism with Chinese Han essential hypertension

Cited by 17 publications

References 9 publications

Lack of Association of ACE2 G8790A Gene Mutation with Essential Hypertension in the Chinese Population: A Meta-Analysis Involving 5260 Subjects

Lack of Association of ACE2 G8790A Gene Mutation with Essential Hypertension in the Chinese Population: A Meta-Analysis Involving 5260 Subjects

From gene to proteinâ€”experimental and clinical studies of ACE2 in blood pressure control and arterial hypertension

ACE2: Angiotensin II/Angiotensin-(1–7) Balance in Cardiac and Renal Injury

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