Review: association between angiotensin converting enzyme G2350A polymorphism and hypertension risk: a meta-analysis

J Renin Angiotensin Aldosterone Syst. 2011 Mar;12(1):8-14. doi: 10.1177/1470320310375859. Epub 2010 Jul 16.

Abstract

Background and objective: An exonic polymorphism G2350A (rs4343) in angiotensin converting enzyme (protein: ACE; gene: ACE) was shown to exert the most significant influence on plasma ACE levels. We therefore performed a meta-analysis to investigate association of ACE G2350A polymorphism with hypertension.

Methods: Published case-control studies in English were identified. A total of four studies with 1699 cases and 1274 controls were identified. A random-effects model was performed irrespective of the between-study heterogeneity. Study quality was assessed in duplicate.

Results: Compared with 2350G, the ACE 2350A allele conferred a protective effect on hypertension (odds ratio (OR) = 0.81; 95% confidence interval (CI), 0.56-1.18; p = .28). Similarly, comparisons of 2350AA and 2350GA with 2350GG generated a nonsignificant reduced risk, respectively. Under the dominant model, the ACE 2350A allele conferred a reduced hypertension risk and such associations were divergent between Han Chinese and Muslims from the Arab Gulf and Pakistan. Under the recessive model, this protective effect was totally reversed (OR = 1.01; 95% CI, 0.77-1.33; p = .94). Subgroup analyses indicated a significant protective effect of ACE 2350A compared with 2350G among Muslims from the Arab Gulf and Pakistan (OR = 0.55; 95% CI, 0.42-0.71; p < .00001). No publication biases were observed.

Conclusions: Our results demonstrate that the ACE 2350A allele is associated with a significantly reduced hypertension risk among Muslims from the Arab Gulf and Pakistan, yet an elevated risk among Han Chinese.

Publication types

  • Meta-Analysis
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Genetic Association Studies*
  • Genetic Predisposition to Disease*
  • Humans
  • Hypertension / genetics*
  • Middle Aged
  • Peptidyl-Dipeptidase A / genetics*
  • Polymorphism, Single Nucleotide / genetics*
  • Publication Bias
  • Risk Factors

Substances

  • Peptidyl-Dipeptidase A