Deletion Polymorphisms in the Angiotensin Converting Enzyme Gene Are Associated with Pulmonary Hypertension Evoked by Exercise Challenge in Patients with Chronic Obstructive Pulmonary Disease

Kanazawa, Hiroshi; Okamoto, Takashi; Hirata, Kazuto; Yoshikawa, Junichi

doi:10.1164/ajrccm.162.4.9909120

Cited by 90 publications

(75 citation statements)

References 17 publications

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“…To address this hypothesis, it is important that future studies undertake the assessment of both muscle strength and endurance in combination with muscle biopsy analysis of fiber types (Harry et al, 2004). Kanazawa et al (2000) suggested that the I/D polymorphism in the ACE gene may be associated with pulmonary hypertension evoked by exercise challenge in patients with COPD. Similarly, Tkacova et al (2005) noted that increases in pulmonary artery pressure in patients with COPD are related to the ACE I/D polymorphism.…”

Section: Discussionmentioning

confidence: 99%

The insertion/deletion polymorphism in the ACE gene and chronic obstructive pulmonary disease

Şimşek

Tekeş²,

Oral³

et al. 2013

Genet. Mol. Res.

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ABSTRACT. An insertion/deletion (I/D) polymorphism was identified in intron 16 of the gene encoding the human angiotensin I-converting enzyme (ACE), a candidate gene for chronic obstructive pulmonary disease (COPD). We investigated the relationship between this polymorphism in the ACE gene and the risk of developing COPD. Sixty-six COPD in-patients and 40 non-smoking control individuals were recruited for this study. The distribution of ACE genotypes in these individuals was studied. The frequencies of ACE genotypes were found to be 47.0% for DD, 30.3% for ID, and 22.7% for II in the COPD group and 32.5% for DD, 47.5% for ID, and 20.0% for II in the control group. The allele frequencies were found to be 0.62% for the D allele and 0.38% for the I allele in the COPD group and 0.56% for the D allele and 0.44% for the I allele in the control group. A significant difference ACE gene and chronic obstructive pulmonary disease was found between I and D allele frequencies (P < 0.05) of the study and control groups. Our results suggest that this ACE polymorphism may be associated with the development of COPD.

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Section: Discussionmentioning

confidence: 99%

The insertion/deletion polymorphism in the ACE gene and chronic obstructive pulmonary disease

Şimşek

Tekeş²,

Oral³

et al. 2013

Genet. Mol. Res.

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show abstract

“…Several studies have investigated the association between ACE activity and OSAHS (Rohatgi, 1982;Kanazawa et al, 2000;Barcelo et al, 2001) but the results are inconsistent. A correlation between homozygous gene deletion (DD genotype) and high ACE activity has been reported in many studies (Ozen et al, 1997;Seckin et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

Meta-analysis demonstrates lack of association between the ACE gene I/D polymorphism and obstructive sleep apnea-hypopnea syndrome occurrence and severity

Feng¹,

Ri²,

Wan³

et al. 2013

Genet. Mol. Res.

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ABSTRACT. Published data on a possible association between the angiotensin-converting enzyme (ACE) gene I/D polymorphism and obstructive sleep apnea-hypopnea syndrome (OSAHS) occurrence and its severity risk are inconclusive. We performed a meta-analysis of case-control studies published in English or Chinese. Thirteen studies, totaling 1361 cases and 1373 controls, were investigated for association of the ACE I/D polymorphism with OSAHS. We also made a study of ACE I/D with OSAHS severity risk, including 879 mild/moderate OSAHS patients and 357 severe OSAHS patients. A random-effects model was used, irrespective of between-study heterogeneity. Study quality was assessed in duplicate. Overall, the ACE I/D polymorphism was not significantly associated with an increase in OSAHS risk [odds ratio (OR) = 1.21; 95% confidence interval (95%CI) = 0.88-1.65; P = 0.24]. In subgroup analysis by ethnicity, comparison of alleles I with D demonstrated a 58% (nonsignificantly) increased risk for OSAHS in Chinese (OR = 1.58; 95%CI = 0.92-2.70; P = 0.09). We also found that there was no significant association between ACE I/D and OSAHS severity risk. No publication biases were observed. This meta-analysis suggests that there is no significantly increased risk for OSAHS occurrence or severity associated with the ACE I/D polymorphism.

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“…[32][33][34][35][36][37][38][39][40] Some, but not all, of these studies emanate from clinical trials of exercise, diet or drug treatment interventions on blood pressure regulation. The most widely studied gene in this context is the angiotensinogen I-converting enzyme gene (ACE).…”

Section: Gene-environment Interactionmentioning

confidence: 99%

“…Studies examining the modifying roles of ACE genotypes on blood pressure response to exercise have focused primarily on the effects of acute exercise often in relatively small samples. [32][33][34][35][36][37][38][39] At least two medium-to long-term clinical trials from North America 37 and Finland 40 have reported on the association between ACE genotypes and blood pressure responses to long-term aerobic exercise training. In the North American HERITAGE study, Rankinen and colleagues examined the blood pressure response by ACE I/D and M235T genotypes to an exercise stress test before and after 20 weeks of aerobic exercise training.…”

Section: Gene-environment Interactionmentioning

confidence: 99%

Identifying genes for primary hypertension: methodological limitations and gene–environment interactions

Franks

2008

J Hum Hypertens

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Hypertension segregates within families, indicating that genetic factors explain some of the variance in the risk of developing the disease; however, even with major advances in genotyping technologies facilitating the discovery of multiple genetic risk markers for cardiovascular and metabolic diseases, little progress has been made in defining the genetic defects that cause elevations in blood pressure. Several plausible explanations exist for this apparent paradox, one of which is that the risk conveyed by genes involved in the development of hypertension is context dependent. This notion is supported by a growing number of published animal and human studies, although none has yet provided unequivocal evidence that genetic and environmental factors interact to influence the risk of primary hypertension in humans. In this review, an assumption is made that common genetic variation contributes meaningfully to the development of primary hypertension. The review focuses on (i) several methodological limitations of genetic association studies and (ii) the roles that geneenvironment interactions might play in the development of primary hypertension. The proceeding sections of the review examine the design features necessary for future studies to adequately test the hypothesis that genes for primary hypertension act in a context-dependent manner. Finally, an outline of how knowledge of gene-environment interactions might be used to optimize the prevention or treatment of primary hypertension is provided.

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Deletion Polymorphisms in the Angiotensin Converting Enzyme Gene Are Associated with Pulmonary Hypertension Evoked by Exercise Challenge in Patients with Chronic Obstructive Pulmonary Disease

Cited by 90 publications

References 17 publications

The insertion/deletion polymorphism in the ACE gene and chronic obstructive pulmonary disease

The insertion/deletion polymorphism in the ACE gene and chronic obstructive pulmonary disease

Meta-analysis demonstrates lack of association between the ACE gene I/D polymorphism and obstructive sleep apnea-hypopnea syndrome occurrence and severity

Identifying genes for primary hypertension: methodological limitations and gene–environment interactions

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