{"title":"Angiotensin-converting enzyme insertion/deletion polymorphism associated with allergic rhinitis susceptibility: evidence from 1410 subjects.","authors":"Hai Lin, Dong Lin, Chun-Quan Zheng","doi":"10.1177/1470320313502107","DOIUrl":"https://doi.org/10.1177/1470320313502107","url":null,"abstract":"<p><strong>Background and objective: </strong>Whether the insertion/deletion (I/D) polymorphism of the angiotensin-converting enzyme (ACE) gene increases susceptibility to allergic rhinitis (AR) is still undetermined. Therefore, this meta-analysis was performed to systematically assess the possible association between them.</p><p><strong>Methods: </strong>The OVID, Medline, Embase, Web of Science, CNKI and Wangfang databases were searched to identify the eligible studies focusing on the association between ACE I/D polymorphism and susceptibility to AR.</p><p><strong>Results: </strong>A total of 1410 subjects from six studies were subjected to meta-analysis. In the overall analysis, ACE I/D polymorphism had a statistically significant association with increased AR risk under all genetic models (p<0.05). In the subgroup analysis by ethnicity, significant elevated AR risks were associated with ACE I/D polymorphism in Asians under all genetic models (p<0.05) and in Caucasians under under allele contrast, homozygous comparison and recessive models (p<0.05). In the subgroup analysis by age, ACE I/D polymorphism was associated with significant elevated risks of AR in adults (p<0.05) but not in children (p>0.05) under all genetic models.</p><p><strong>Conclusions: </strong>The ACE I/D polymorphism may be a risk factor for AR and studies with large sample size and representative population are warranted to verify this finding.</p>","PeriodicalId":520698,"journal":{"name":"Journal of the renin-angiotensin-aldosterone system : JRAAS","volume":" ","pages":"593-600"},"PeriodicalIF":2.9,"publicationDate":"2014-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1470320313502107","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40259979","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yan Zhang, Teng-Yue Diao, Sa-Sa Gu, Shu-Yan Wu, Yoseph A Gebru, Xi Chen, Jing-Yu Wang, Shu Ran, Man-Sau Wong
{"title":"Effects of angiotensin II type 1 receptor blocker on bones in mice with type 1 diabetes induced by streptozotocin.","authors":"Yan Zhang, Teng-Yue Diao, Sa-Sa Gu, Shu-Yan Wu, Yoseph A Gebru, Xi Chen, Jing-Yu Wang, Shu Ran, Man-Sau Wong","doi":"10.1177/1470320312471229","DOIUrl":"https://doi.org/10.1177/1470320312471229","url":null,"abstract":"<p><strong>Introduction: </strong>This study was performed to address the pathological roles of the skeletal renin-angiotensin system (RAS) in type 1 diabetes-induced osteoporosis and the effects of the angiotensin II type 1 receptor blocker losartan on bones in diabetic mice.</p><p><strong>Materials and methods: </strong>Bone histomorphology was detected by H&E staining, Safranin O staining and X-ray radiography. Micro-CT was performed for the analysis of bone parameters. Gene and protein expression were determined by RT-PCR and immunoblotting.</p><p><strong>Results: </strong>Type 1 diabetic mice displayed osteopenia phenotype, and losartan treatment had no osteoprotective effects on diabetic mice as shown by the reduction of bone mineral density and microarchitectural parameters at the proximal metaphysis of the tibia. The mRNA expression of AGT, renin receptor and ACE, and protein expression of renin and AT1R were markedly up-regulated in the bones of vehicle-treated diabetic mice compared to those of non-diabetic mice. The treatment with losartan further significantly increased the expression of AGT, renin, angiotensin II and AT1R, and reduced the expression of AT2R receptor as compared to those of diabetic mice.</p><p><strong>Conclusion: </strong>Local bone RAS functionally played a role in the development of type 1 diabetic osteoporosis, and losartan had no bone-sparing function in diabetes mice because of enhance skeletal RAS activity.</p>","PeriodicalId":520698,"journal":{"name":"Journal of the renin-angiotensin-aldosterone system : JRAAS","volume":" ","pages":"218-27"},"PeriodicalIF":2.9,"publicationDate":"2014-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1470320312471229","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40206077","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The M235T polymorphism in the angiotensinogen gene and myocardial infarction risk: a meta-analysis.","authors":"Yu-Jing Wang, Yan Pan","doi":"10.1177/1470320312471148","DOIUrl":"https://doi.org/10.1177/1470320312471148","url":null,"abstract":"<p><strong>Objective: </strong>The angiotensinogen (AGT) gene M235T polymorphism has been reported to be associated with myocardial infarction (MI), but previous studies have been inconsistent. The present study aimed at assessing the association of M235T polymorphism in the AGT gene with MI using a meta-analysis.</p><p><strong>Methods: </strong>We retrieved literature in Google Scholar, PubMed, Cochrane Library and the China National Knowledge Infrastructure database (January 1990-December 2011) for the relevant studies on the AGT polymorphism M235T and risk of MI. Statistical analyses were carried out using Stata 10.0 for combining all the relevant studies. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of the association. Begg's test was used to measure publication bias.</p><p><strong>Results: </strong>A total of 21 case-control studies containing 5887 patients and 6164 controls were enrolled into this meta-analysis. Overall, significant association was found between the AGT gene M235T polymorphism and risk of MI in the subgroup analysis for TT vs MT in Asians (OR 1.47, 95% CI: 1.01-2.12; p = 0.04). No associations were detected between AGT M235T and the risk of MI in total population and Caucasians.</p><p><strong>Conclusions: </strong>This meta-analysis demonstrated that the AGT M235T polymorphism could be a prediction marker for risk of MI in Asians. Conclusive evidence on the effects of the variants in MI should be addressed in further studies.</p>","PeriodicalId":520698,"journal":{"name":"Journal of the renin-angiotensin-aldosterone system : JRAAS","volume":" ","pages":"294-300"},"PeriodicalIF":2.9,"publicationDate":"2014-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1470320312471148","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40206078","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Left ventricular remodelling after acute myocardial infarction: impact of clinical, echocardiographic parameters and polymorphism of angiotensinogen gene.","authors":"Diana Zaliaduonyte-Peksiene, Sandrita Simonyte, Vaiva Lesauskaite, Jolanta Vaskelyte, Olivija Gustiene, Vaida Mizariene, Renaldas Jurkevicius, Giedre Jariene, Abdonas Tamosiunas, Remigijus Zaliunas","doi":"10.1177/1470320312471228","DOIUrl":"https://doi.org/10.1177/1470320312471228","url":null,"abstract":"<p><strong>Introduction: </strong>The development of left ventricular remodelling after acute myocardial infarction is a predictor of heart failure and mortality. The purpose of the present study was to assess whether the polymorphism of angiotensinogen (AGT) gene with threonine (T) instead of methionine (M) at amino acid 235 in exon 2 (M235T) had effects on cardiac remodelling after acute myocardial infarction.</p><p><strong>Methods: </strong>One hundred and forty-one patients (mean age 56.4±11.1 years) with a first acute myocardial infarction were enrolled. Within 24-72 hours of the onset of the symptoms and at a four month period two-dimensional echocardiography was performed. Remodelling was defined as a 20% increase from the baseline in left ventricular end-diastolic volume. The genotypes of the study group were compared with the reference group (n=1010) genotypes. AGT M235T polymorphism was determined using polymerase chain reaction amplification.</p><p><strong>Results: </strong>At follow-up, 49 patients (34.7%) were classified as having left ventricular remodelling. Anterior localization of the infarct (p=0.008), leucocyte count at admission (p=0.040), global left ventricular longitudinal strain (p=0.021) and MM genotype of AGT (p=0.024) were independent predictors of ventricular remodelling after myocardial infarction.</p><p><strong>Conclusions: </strong>Anterior wall infarction, increased leucocyte count, decreased longitudinal strain of left ventricular and polymorphism of AGT M235T may predict remodelling after myocardial infarction.</p>","PeriodicalId":520698,"journal":{"name":"Journal of the renin-angiotensin-aldosterone system : JRAAS","volume":" ","pages":"286-93"},"PeriodicalIF":2.9,"publicationDate":"2014-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1470320312471228","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40206822","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Angiotensin-converting enzyme I/D gene polymorphism affects early cardiac response to professional training in young footballers.","authors":"Maha M Saber-Ayad, Yasser S Nassar, Inas A Latif","doi":"10.1177/1470320312471150","DOIUrl":"https://doi.org/10.1177/1470320312471150","url":null,"abstract":"<p><strong>Background: </strong>The renin-angiotensin-aldosterone system plays a role in physiological and pathological responses of the heart to both static and dynamic exercise. Previous studies showed that the level of angiotensin II is determined by the angiotensin-converting enzyme insertion/deletion (ACE I/D) polymorphism.</p><p><strong>Aim: </strong>We aimed in this study to determine the effect of ACE I/D gene polymorphism on the extent of functional and structural cardiac changes in response to one year of professional football training in young footballers.</p><p><strong>Methods and results: </strong>We studied 68 young male football players and a comparable control group. Besides medical history and clinical examination, 12 lead ECG and transthoracic 2D echocardiography examination were performed. Genotyping of ACE was analyzed using PCR-based technique. There was no statistically significant difference in distribution of genotypes among athletes compared with control subjects. D allele showed a graded effect on both EF (73.55, 67.5 and 60.2%, p=0.03) and PASP (37.6, 26.1 and 21.39 mmHg, p=0.02) in DD, ID and II subjects, respectively.</p><p><strong>Conclusion: </strong>Early cardiac changes in young footballers can be affected by ACE I/D polymorphism. There is a summative effect of the D allele in increasing EF and PASP in response to professional football training.</p>","PeriodicalId":520698,"journal":{"name":"Journal of the renin-angiotensin-aldosterone system : JRAAS","volume":" ","pages":"236-42"},"PeriodicalIF":2.9,"publicationDate":"2014-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1470320312471150","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40206080","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Sung Joon Shin, ChiYeon Lim, Sang Woo Oh, Moo-Yong Rhee
{"title":"The unique response of renin and aldosterone to dietary sodium intervention in sodium sensitivity.","authors":"Sung Joon Shin, ChiYeon Lim, Sang Woo Oh, Moo-Yong Rhee","doi":"10.1177/1470320314526437","DOIUrl":"https://doi.org/10.1177/1470320314526437","url":null,"abstract":"<p><strong>Introduction: </strong>Sodium sensitivity (SS) is a phenomenon in which significant changes in blood pressure (BP) are observed based on sodium intake. The renin-angiotensin-aldosterone system plays a critical role in sodium handling and hypertension. We identified the specific responses of renin and aldosterone based on dietary sodium intake and revealed the relationship between these hormonal changes and dietary sodium intake in patients with SS.</p><p><strong>Materials and methods: </strong>In total, 61 subjects were available to analyze full data including plasma renin activity (PRA) and aldosterone. Participants were given a low-sodium DASH diet (LSD) for 7 days and a high-sodium DASH diet (HSD) for the following 7 days.</p><p><strong>Results: </strong>SS was found in five (14.71%) in normotensives, and 14 (51.85%) in hypertensives. In sodium-resistant (SR) subjects, both PRA and aldosterone decreased significantly after consuming HSD. Moreover, a significant correlation was observed between PRA and aldosterone in SR subjects. In contrast, only hypertensive subjects showed a marked fall in PRA after consuming HSD (1.299 ± 0.904 vs. 0.593 ± 0.479) among SS subjects.</p><p><strong>Conclusions: </strong>This study demonstrated the different responses of renin and aldosterone in SS and SR subjects based on dietary sodium intake whether or not they had hypertension.</p>","PeriodicalId":520698,"journal":{"name":"Journal of the renin-angiotensin-aldosterone system : JRAAS","volume":" ","pages":"117-23"},"PeriodicalIF":2.9,"publicationDate":"2014-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1470320314526437","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40304786","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Cholecalciferol administration blunts the systemic renin-angiotensin system in essential hypertensives with hypovitaminosis D.","authors":"Davide Carrara, Matteo Bernini, Alessandra Bacca, Ilaria Rugani, Emiliano Duranti, Agostino Virdis, Lorenzo Ghiadoni, Stefano Taddei, Giampaolo Bernini","doi":"10.1177/1470320312471149","DOIUrl":"https://doi.org/10.1177/1470320312471149","url":null,"abstract":"<p><strong>Introduction: </strong>Vitamin D plasma levels are negatively associated with blood pressure and cardiovascular mortality, and vitamin D supplementation reduces cardiovascular events. Renin-angiotensin system (RAS) suppression may be one of the mechanisms involved. However, there are no interventional prospective studies demonstrating a reduction in circulating RAS components after vitamin D treatment.</p><p><strong>Methods: </strong>Fifteen consecutive drug-free patients with essential hypertension and hypovitaminosis D underwent therapy with an oral dose of 25000 I.U. of cholecalciferol once a week for two months, while maintaining a constant-salt diet. In basal conditions and at the end of the study, RAS activity (plasma angiotensinogen, renin, PRA, angiotensin II, aldosterone and urinary angiotensinogen) was investigated, in addition to blood pressure and plasma vitamin D levels (25(OH)D).</p><p><strong>Results: </strong>After cholecalciferol administration, all patients exhibited normalized plasma 25(OH)D values. At the end of the study, a reduction (p < 0.05) in plasma renin and aldosterone, and a decrement, although not significant, of PRA and angiotensin II, was observed. No difference was found in plasma and urinary angiotensinogen or blood pressure values.</p><p><strong>Conclusions: </strong>Our data indicate that in essential hypertensives with hypovitaminosis D, pharmacological correction of vitamin D levels can blunt systemic RAS activity.</p>","PeriodicalId":520698,"journal":{"name":"Journal of the renin-angiotensin-aldosterone system : JRAAS","volume":" ","pages":"82-7"},"PeriodicalIF":2.9,"publicationDate":"2014-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1470320312471149","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40206079","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Rupinder Kaur, Reena Das, Jasmina Ahluwalia, Rohit Manoj Kumar, K K Talwar
{"title":"Synergistic effect of angiotensin II type-1 receptor 1166A/C with angiotensin-converting enzyme polymorphism on risk of acute myocardial infarction in north Indians.","authors":"Rupinder Kaur, Reena Das, Jasmina Ahluwalia, Rohit Manoj Kumar, K K Talwar","doi":"10.1177/1470320312438789","DOIUrl":"https://doi.org/10.1177/1470320312438789","url":null,"abstract":"<p><strong>Introduction: </strong>This first study from north India investigated the synergistic effect of AT1R 1166A/C with the ACE I/D polymorphism on risk of acute myocardial infarction (AMI).</p><p><strong>Materials and methods: </strong>Traditional coronary risk factors, ACE I/D and AT1R 1166A/C polymorphism were analyzed in 350 patients with AMI and 350 matched controls.</p><p><strong>Results: </strong>In univariate analysis, hypertension (52.9% vs. 11.1%; OR=8.9; 95%CI 6.0-13.3), diabetes mellitus (16.0% vs. 0.6%; OR=33.1; 95%CI 8.0-137), smoking (43.7% vs. 20.9%; OR=2.9; 95%CI 2.1-4.1), family history of coronary artery disease (22.3% vs. 14.0%; OR=1.8; 95%CI 1.2-2.6), high body mass index (64.3% vs. 51.4%; OR=1.7; 95%CI 1.3-2.3), high waist-hip ratio (46.2% vs. 2.3%; OR=37; 95%CI 16-85.8) and AT1R 1166AC genotype (20.6% vs. 12%; OR=1.9; 95%CI 1.3-2.9) were associated with AMI. In multivariate analysis, all these factors were found to be independent risk predictors for AMI. Subjects carrying the AT1R 1166AC+CC and ACE ID+DD combined genotype showed a twofold increased association (OR=2.1; 95%CI 1.2-3.5) compared with the AT1R 1166AA-ACE II combined genotype. Patients who smoked and who carried the ACE ID+DD genotype had 2.4-fold (OR=2.4; 95%CI 1.5-3.8), and with the AT1R 1166AC+CC genotype had 15-fold (OR=14.9; 95%CI 5.2-42.8) increased risk of AMI compared with non-smoking non-carriers.</p><p><strong>Conclusions: </strong>The AT1R 1166A/C polymorphism has association with AMI among north Indian patients, particularly if integrated with ACE I/D polymorphism and smoking.</p>","PeriodicalId":520698,"journal":{"name":"Journal of the renin-angiotensin-aldosterone system : JRAAS","volume":" ","pages":"440-5"},"PeriodicalIF":2.9,"publicationDate":"2012-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1470320312438789","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40143336","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Domenico Galzerano, Sara Di Michele, Giuseppe Paolisso, Bernardino Tuccillo, Diana Lama, Sabino Carbotta, Antonio Cittadini, Michele Adolfo Tedesco, Carlo Gaudio
{"title":"A multicentre, randomized study of telmisartan versus carvedilol for prevention of atrial fibrillation recurrence in hypertensive patients.","authors":"Domenico Galzerano, Sara Di Michele, Giuseppe Paolisso, Bernardino Tuccillo, Diana Lama, Sabino Carbotta, Antonio Cittadini, Michele Adolfo Tedesco, Carlo Gaudio","doi":"10.1177/1470320312443909","DOIUrl":"https://doi.org/10.1177/1470320312443909","url":null,"abstract":"<p><strong>Introduction: </strong>Atrial remodelling, leading to atrial fibrillation (AF), is mediated by the renin-angiotensin-aldosterone system.</p><p><strong>Methods: </strong>Mild hypertensive outpatients (systolic/diastolic blood pressure 140-159/90-99 mmHg) in sinus rhythm who had experienced ≥ 1 electrocardiogram (ECG)-documented AF episode in the previous six months received randomly telmisartan 80 mg/day or carvedilol 25 mg/day. Blood pressure and 24-hour ECG were monitored monthly for one year; patients were asked to report symptomatic AF episodes and to undergo an ECG as early as possible.</p><p><strong>Results: </strong>One hundred and thirty-two patients completed the study (telmisartan, n=70; carvedilol, n=62). Significantly fewer AF episodes were reported with telmisartan versus carvedilol (14.3% vs. 37.1%; p<0.003). Left atrial diameter, assessed by echocardiography, was similar with telmisartan and carvedilol (3.4±2.3 cm vs. 3.6±2.4 cm). At study end, both regimes significantly reduced mean left ventricular mass index, but the reduction obtained with telmisartan was significantly greater than with carvedilol (117.8±10.7 vs. 124.7±14.5; p<0.0001). Mean blood pressure values were not significantly different between the groups (telmisartan 154/97 to 123/75 mmHg; p<0.001; carvedilol 153/94 to 125/78 mmHg; p<0.001).</p><p><strong>Conclusions: </strong>Telmisartan was significantly more effective than carvedilol in preventing recurrent AF episodes in hypertensive AF patients, despite a similar lowering of blood pressure.</p>","PeriodicalId":520698,"journal":{"name":"Journal of the renin-angiotensin-aldosterone system : JRAAS","volume":" ","pages":"496-503"},"PeriodicalIF":2.9,"publicationDate":"2012-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1470320312443909","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40194154","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Min Gao, Yuli Wang, Yuzhi Shi, Dan Liu, Yin Liang, Yan Yu, Jiahui Zhaobin, Lili Zhu, Shoude Jin
{"title":"The relationship between three well-characterized polymorphisms of the angiotensin converting enzyme gene and lung cancer risk: a case-control study and a meta-analysis.","authors":"Min Gao, Yuli Wang, Yuzhi Shi, Dan Liu, Yin Liang, Yan Yu, Jiahui Zhaobin, Lili Zhu, Shoude Jin","doi":"10.1177/1470320312443912","DOIUrl":"https://doi.org/10.1177/1470320312443912","url":null,"abstract":"<p><strong>Background and objective: </strong>The gene encoding angiotensin converting enzyme (ACE) is a promising candidate for lung cancer. We aimed to assess three well-characterized polymorphisms of the ACE gene (A-240T, I/D, A2350G) and lung cancer in Chinese people, and complete a meta-analysis of the association of I/D polymorphism with lung cancer.</p><p><strong>Methods and results: </strong>In our case-control study, a total of 684 patients with lung cancer and 602 age-matched controls were recruited. Genotyping was performed using polymerase chain reaction (PCR) and ligase detection reactions (LDR) techniques. Single-locus analysis indicated that carriers of the A-240T allele had a significantly increased risk for lung cancer under additive (odds ratio (OR)=1.2; 95% confidence interval (CI): 1.02-1.42; P=0.027) and recessive (OR=1.8; 95% CI: 1.24-2.63; P=0.002) models, and that DD genotype carriers were 1.97 times more likely to develop lung cancer (95% CI: 1.25-3.11; P=0.004) compared with those with the I allele under the recessive model. However, no significance was observed in further haplotype analysis (P>0.05). In a meta-analysis of ACE gene insertion-deletion (I/D) polymorphism from six studies with 1183 lung cancer patients and 1065 controls, we failed to detect any significant association (overall OR=1.09; 95% CI: 0.84-1.41). A low probability of publication bias was observed.</p><p><strong>Conclusions: </strong>Our results suggest that ACE gene A-240T polymorphism might be a genetic marker for the development of lung cancer in Chinese people.</p>","PeriodicalId":520698,"journal":{"name":"Journal of the renin-angiotensin-aldosterone system : JRAAS","volume":" ","pages":"455-60"},"PeriodicalIF":2.9,"publicationDate":"2012-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1470320312443912","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40186372","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}