Impact of I/D polymorphism of ACE gene on risk of development and course of chronic obstructive pulmonary disease

Mlak, Radosław; Homa‐Mlak, Iwona; Powrózek, Tomasz; Maćkiewicz, Barbara; Michnar, Marek; Krawczyk, Paweł; Dziedzic, Marcin; Rubinsztajn, Renata; Chazan, Ryszarda; Milanowski, Janusz; Małecka‐Massalska, Teresa

doi:10.5114/aoms.2015.50757

Cited by 10 publications

(6 citation statements)

References 26 publications

(29 reference statements)

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“…One study was rejected because it was an animal experiment, and another article was not included in the meta-analysis because it was not designed as a case–control study. Finally, we confirmed 15 eligible studies (1,279 cases and 1,356 controls) 7 , 10 , 11 , 13 , 15 – 25 for the COPD subgroup and four studies for the PH subgroup, and we included them in the current meta-analysis. Twelve articles were in English, 7 , 10 , 11 , 13 , 15 – 20 , 23 , 25 and three were in Chinese.…”

Section: Resultsmentioning

confidence: 93%

<em>ACE</em> gene polymorphism is associated with COPD and COPD with pulmonary hypertension: a meta-analysis

Ma¹,

Xiang²,

Liu³

et al. 2018

COPD

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PurposeAngiotensin-converting enzyme (ACE) gene I/D polymorphism has been studied in relation to the susceptibility to COPD and COPD with pulmonary hypertension (PH) with inconclusive results. We performed the first comprehensive meta-analysis to evaluate accurately the association between the ACE gene polymorphism and the risk of COPD.MethodsData were analyzed using odds ratios (ORs) and the corresponding 95% CIs to measure the strength of the models. Subgroup analyses were conducted by ethnicity and complication which referred to PH.ResultsIn total, 15 studies (2,635 participants) were included in our study, of which four studies (288 participants) were for PH subgroup. The overall analysis results indicated that the ACE gene polymorphism was not associated with COPD susceptibility in all gene models. However, the ethnic subgroup analysis results indicated that ACE gene polymorphism was associated with Asians’ susceptibility to COPD (DD+DI vs II, OR=1.47, P=0.019, 95% CI: 1.07–2.02). Further, the overall results of the present study detected no statistical significance between ACE gene polymorphism and the risk of COPD with PH, but the homozygote variant (DD) increased the risk of PH in Asian COPD patients (DD vs ID+II, OR=2.05, P=0.05, 95% CI: 1.00–4.19).ConclusionThe current study suggests that ACE polymorphism, particularly the homozygote variant (DD), might contribute to the risk of COPD and COPD with PH among Asians. Further studies with larger sample size and more ethnicities are expected to be conducted in the future to validate the results.

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Section: Resultsmentioning

confidence: 93%

<em>ACE</em> gene polymorphism is associated with COPD and COPD with pulmonary hypertension: a meta-analysis

Ma¹,

Xiang²,

Liu³

et al. 2018

COPD

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“…Our initial search of three public databases identified 42 articles published in the English language, and only 16 of them were eligible for analysis. 6 – 9 , 13 – 24 There were 12 articles (12 studies including 2113 patients and 8786 controls) that incorporated data on the risk of the ACE gene I/D polymorphism for COPD, and eight articles (14 studies including 11,664 subjects) that incorporated data on the changes of either FEV 1 or FEV 1 /FEV or circulating ACE across the genotypes of this polymorphism.…”

Section: Resultsmentioning

confidence: 99%

Association of angiotensin-converting enzyme gene I/D polymorphism with chronic obstructive pulmonary disease: a meta-analysis

Fan

Sun

et al. 2018

J Renin Angiotensin Aldosterone Syst

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Objectives:We conducted a meta-analysis of published studies on the angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism associated with the risk of chronic obstructive pulmonary disease, as well as with pulmonary function and circulating angiotensin-converting enzyme changes.Methods:A literature search, quality assessment and data extraction were completed independently and in duplicate.Results:A total of 16 articles were meta-analysed, including 12 articles (2113 patients and 8786 controls) for chronic obstructive pulmonary disease risk and eight articles (11,664 subjects) for pulmonary and circulating phenotypes. In overall and subgroup analyses, no significance was noted between the I/D polymorphism and chronic obstructive pulmonary disease risk under all genetic models (P>0.05), without heterogeneity or publication bias. Carriers of II, ID and II plus ID genotypes had significantly lower levels of circulating angiotensin-converting enzyme than those with the DD genotype (weighted mean difference −13.35, −8.13 and −10.74 U/L, respectively, P<0.001). For forced expiratory volume in one second (FEV1)/forced vital capacity, carriers of the DD genotype had marginally lower levels than those with the DD genotype (weighted mean difference –1.66, P=0.034). Furthermore in the case of FEV1 of 50% or greater of predicted FEV1, FEV1 was marginally lower in ID genotype carriers than DD genotype carriers (weighted mean difference −3.50, P=0.056).Conclusions:Our meta-analytical findings demonstrated that the ACE gene I/D polymorphism was not associated with the risk of chronic obstructive pulmonary disease.

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“…Individuals with allele C for rs4588 in the GC gene showed a higher exacerbation frequency, higher susceptibility to COPD, emphysema, and a tendency toward a rapid decrease of airflow obstruction 168 . The minor allele of SNP rs2227744G > A in the proteaseactivated receptor 1 (F2R) was associated with protection against frequent exacerbations 169 , while genotype DD of the gene ACE was associated with a lower risk in males 170 .…”

Section: Genetic Considerations In Copd Exacerbationsmentioning

confidence: 99%

Role of Genetic Susceptibility in Nicotine Addiction and Chronic Obstructive Pulmonary Disease

Pérez-Rubio

Córdoba-Lanús

Cupertino

et al. 2019

RIC

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Chronic obstructive pulmonary disease (COPD) is a leading cause of morbidity and mortality in developed countries. Although cigarette smoking is the major risk factor, only 10-20% of smokers develop COPD. The extent of cigarette smoking (pack-years and smoking duration) accounts for only 15% of the variation in lung function, indicating that differences in susceptibility to COPD must exist. We provide an overview of the complexity of nicotine addiction and COPD, with special attention to the involvement of genetic factors. The following aspects are discussed in the present article: (1) epidemiology in Mexico and (2) a review of the published literature on genetic association studies using the National Center for Biotechnology Information database of the United States as a search tool. COPD is unique among complex genetic diseases where an environmental risk factor is known and the level of exposure can be documented with some precision. The high morbidity and mortality associated with COPD and its chronic and progressive nature has prompted the use of molecular genetic studies to identify susceptibility factors for the disease. Biomedical research has a remarkable set of tools to aid in the discovery of genes and polymorphisms. We present a review of the most relevant genetic associations in nicotine addiction and COPD.

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Impact of I/D polymorphism of ACE gene on risk of development and course of chronic obstructive pulmonary disease

Cited by 10 publications

References 26 publications

<em>ACE</em> gene polymorphism is associated with COPD and COPD with pulmonary hypertension: a meta-analysis

<em>ACE</em> gene polymorphism is associated with COPD and COPD with pulmonary hypertension: a meta-analysis

Association of angiotensin-converting enzyme gene I/D polymorphism with chronic obstructive pulmonary disease: a meta-analysis

Role of Genetic Susceptibility in Nicotine Addiction and Chronic Obstructive Pulmonary Disease

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