FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2037774992> ?p ?o ?g. }

• W2037774992 endingPage "308" @default.
• W2037774992 startingPage "305" @default.
• W2037774992 abstract "Purpose: An insertion/deletion (I/D) polymorphism of the gene for angiotensin-converting enzyme (ACE) is associated with higher ACE plasma levels and activity. This enzyme is known to play an important role in blood pressure regulation and the ACE I/D gene polymorphism has been suggested as a risk factor for atherosclerotic vascular diseases. The purpose of the present study was to investigate a hypothesized association between the ACE I/D polymorphism and retinal artery occlusion (RAO). Methods: A total of 159 patients with RAO and 304 control subjects were enrolled in the present retrospective case-control study. ACE I/D genotypes were determined by polymerase chain reaction. Results: Allelic frequencies and genotype distribution of the ACE I/D polymorphism did not significantly differ between patients and control subjects (ACE DD 25.8% versus 28.0%; p = 0.36). A logistic regression analysis predicted the presence of RAO by arterial hypertension and current smoking status, but not by ACE I/D genotypes. Conclusion: Our data suggest that the ACE I/D polymorphism is not a major risk factor for RAO. Angiotensin I-converting enzyme (ACE) is a carboxypeptidase, which plays a key role in the renin–angiotensin system (RAS) by catalysing the conversion of angiotensin I to vasoactive angiotensin II (AngII) (Ehlers & Riordan 1989; Crisan & Carr 2000). AngII acts as a potent vasoconstrictor, exerts proatherogenic effects and impairs fibrinolysis by increasing plasminogen activator inhibitor type 1 (PAI-1) plasma concentrations (Ridker et al. 1993; van Leeuwen et al. 1994; Feener et al. 1995; Vaughan et al. 1995; Carluccio et al. 2001; Vaughan 2001). Besides its role in the RAS, ACE also affects the kinin–kallikrein system by inactivating bradykinin, a peptide known to promote vasodilatation (Crisan & Carr 2000; Carluccio et al. 2001). Thus, ACE modulates the opposing effects of AngII and bradykinin on the vascular wall haemostasis. Rigat et al. (1990) identified a polymorphism in the ACE gene, which is characterized by the insertion (I) or deletion (D) of a 288 base pair alu repeat sequence within intron 16. This polymorphism has consistently been associated with approximately 45% of the variance of serum ACE concentrations. Homozygotes for the ACE D-allele were found to have ACE levels twice as high as subjects carrying the II genotype (Rigat et al. 1990). Cambien et al. (1992) reported homozygosity for the D-allele as a risk factor for myocardial infarction. Since then, over 300 studies have investigated the role of the ACE I/D gene polymorphism in carotid atherosclerosis, coronary heart disease and stroke (Lindpaintner et al. 1995; Catto et al. 1996; Samani et al. 1996; Zee et al. 1999; Agerholm et al. 2000; Keavney et al. 2000; Tabara et al. 2001). However, their results were controversial and inconclusive. Gori et al. (2004) suggested the ACE I/D gene polymorphism as a novel risk factor for retinal vein occlusion. Its role as a potential risk factor for retinal artery occlusion (RAO), however, has not yet been determined. The purpose of the present study was therefore to test the hypothesis that homozygosity for the ACE I/D gene polymorphism is associated with the presence of RAO. A sample of 159 patients with RAO and 304 control subjects were enrolled in the present retrospective case-control study. Participants were seen at the Department of Ophthalmology, Medical University Graz and gave written informed consent prior to enrolment. The present study was conducted according to the guidelines of the National Gene Technology Act and the local ethics committee. Retinal artery occlusion was diagnosed by ophthalmoscopic fundus examination revealing superficial retinal whitening in the distribution of the involved retinal artery. Exclusion criteria for patients with RAO comprised any history of vasculitis. The control group consisted of 304 subjects who were seen at the Department of Ophthalmology for reasons other than retinal vascular occlusions or vasculitis. Arterial hypertension was defined by a systolic blood pressure ≥ 160 mmHg and/or diastolic blood pressure ≥ 90 mmHg, and/or the current use of antihypertensive drugs. Subjects were classified as diabetes patients if they were being treated for insulin or non-insulin dependent diabetes mellitus. Hypercholesterolemia was defined by a fasting plasma cholesterol level of ≥ 200 mg/dl or the current use of lipid-lowering drugs. Subjects were defined as non-and current smokers according to their smoking status. Genomic DNA was isolated from peripheral blood lymphocytes by standard methods and stored at − 20 °. Genotyping for the ACE polymorphism was performed by size analysis of polymerase chain products as described previously (Tiret et al. 1992). Statistic software spss for Windows, Version 11.0.1, was used for statistical analyses. Metric values were analysed by Student's t-test. Categorical values were compared by chi-squared test. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated by logistic regression analysis. The criterion for statistical significance was p ≤ 0.05. The study group consisted of 159 patients with RAO (66 women and 93 men) and 304 control subjects (132 women and 172 men). The baseline characteristics of patients and control subjects are shown in Table 1. As expected, arterial hypertension and current smokers were found significantly more often among patients with RAO. Genotypes were determined successfully in all participants and genotype distributions did not deviate from those predicted by the Hardy–Weinberg equilibrium. Carriers of the ACE DD genotype were not found significantly more often among patients with RAO than among control subjects (Table 2). Similarly, no significant difference in the D-allele frequency of the ACE I/D gene polymorphism was observed between patients and control subjects (Table 2). Subgroup analysis revealed no significant difference in the prevalences of the DD, ID and II genotypes between patients with central RAO (CRAO) (28.2%, 50.0% and 21.8%, respectively) or branch RAO (BRAO) (23.5%, 48.1% and 28.4%, respectively). The genotype distribution of the ACE I/D polymorphism in control subjects was similar to those previously reported in Central European populations (Friedl et al. 1995; Renner et al. 2002). Logistic regression analysis predicted the presence of RAO by arterial hypertension and current smoking status, but not by homozygosity for the ACE I/D gene polymorphism (Table 3). Additionally, the DD genotype did not predict the presence of arterial hypertension (data not shown). Retinal artery occlusion is one of the leading causes of severe visual impairment among patients older than 60 years. Atherosclerosis, arterial hypertension and hypercholesterolemia have been identified as important risk factors. Only a limited number of cases, however, can be completely explained by the known risk factors alone. Numerous studies have previously investigated the ACE I/D polymorphism as a potential risk factor for cardiovascular diseases. Yet, to the best of our knowledge, the present study is the first to evaluate the role of this polymorphism in patients with RAO. Homozygosity for the ACE I/D polymorphism, which is associated with an approximately twofold increase in ACE activity, was not found significantly more often in patients with RAO compared with control subjects. In a multivariate logistic regression analysis, the ACE DD genotype was associated with a non-significant OR of 0.93 (95% CI 0.59–1.47) for RAO. As a gene−dose effect has been reported for the ACE I/D polymorphism, with the ID genotype showing intermediate and DD homozygotes highest ACE activities, differences in the D-allele frequency between both groups are of interest (Rigat et al. 1990). Yet, no significant difference in the ACE D-allele frequency was observed between patients and control subjects. Separate analysis of patients with BRAO and CRAO revealed a similar genotype distribution, indicating that the ACE I/D gene polymorphism is not a risk factor for either subtype of RAO. Importantly, the present study had an 80% power to exclude an OR ≥ 1.8 for the DD genotype. Thus, our data strongly suggest that the ACE I/D polymorphism does not play an essential role in the pathogenesis of RAO. Arterial hypertension, which is an established risk factor for RAO, was found significantly more often among patients (Blice & Brown 1999). In a logistic regression analysis, arterial hypertension was associated with an OR of 3.34 for RAO. We also analysed a potential association between genotypes of the ACE I/D polymorphism and the presence of arterial hypertension. In agreement with previous reports, the DD genotype was not associated with an increased prevalence of arterial hypertension, indicating that, in contrast to the RAS, the ACE DD genotype is not a major determinant of arterial hypertension (Cambien et al. 1992; Jeunemaitre et al. 1992; Iwai et al. 1994; Schunkert 1997). Considering the beneficial effects of ACE inhibitors on arterial blood pressure and cardiovascular risk, the missing relation between genotype and clinical disease could be due to a compensatory mechanism of organisms with lifelong expositions to higher ACE levels. In conclusion, our results indicate that arterial hypertension, but not the ACE I/D polymorphism itself, is a major risk factor for RAO. The authors thank Gabriele Trummer, Manuela Fischl and Christa Wachswender for their excellent technical assistance." @default.
• W2037774992 created "2016-06-24" @default.
• W2037774992 creator A5013901190 @default.
• W2037774992 creator A5027522449 @default.
• W2037774992 creator A5029297245 @default.
• W2037774992 creator A5030905729 @default.
• W2037774992 creator A5031560900 @default.
• W2037774992 creator A5038542046 @default.
• W2037774992 creator A5073504542 @default.
• W2037774992 creator A5086792424 @default.
• W2037774992 creator A5089537116 @default.
• W2037774992 date "2006-05-16" @default.
• W2037774992 modified "2023-09-27" @default.
• W2037774992 title "Angiotensin-converting enzyme insertion/deletion polymorphism and retinal artery occlusion" @default.
• W2037774992 cites W1981152291 @default.
• W2037774992 cites W1983416483 @default.
• W2037774992 cites W1992351338 @default.
• W2037774992 cites W2006441219 @default.
• W2037774992 cites W2007188741 @default.
• W2037774992 cites W2013688320 @default.
• W2037774992 cites W2015707095 @default.
• W2037774992 cites W2021635921 @default.
• W2037774992 cites W2027579450 @default.
• W2037774992 cites W2033240204 @default.
• W2037774992 cites W2043600435 @default.
• W2037774992 cites W2049257368 @default.
• W2037774992 cites W2067263222 @default.
• W2037774992 cites W2073296087 @default.
• W2037774992 cites W2076907458 @default.
• W2037774992 cites W2097532633 @default.
• W2037774992 cites W2102792004 @default.
• W2037774992 cites W2109921650 @default.
• W2037774992 cites W2110782030 @default.
• W2037774992 cites W2134107449 @default.
• W2037774992 cites W2158252240 @default.
• W2037774992 cites W2163510728 @default.
• W2037774992 cites W2329157757 @default.
• W2037774992 doi "https://doi.org/10.1111/j.1600-0420.2006.00656.x" @default.
• W2037774992 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/16704688" @default.
• W2037774992 hasPublicationYear "2006" @default.
• W2037774992 type Work @default.
• W2037774992 sameAs 2037774992 @default.
• W2037774992 citedByCount "2" @default.
• W2037774992 countsByYear W20377749922014 @default.
• W2037774992 countsByYear W20377749922016 @default.
• W2037774992 crossrefType "journal-article" @default.
• W2037774992 hasAuthorship W2037774992A5013901190 @default.
• W2037774992 hasAuthorship W2037774992A5027522449 @default.
• W2037774992 hasAuthorship W2037774992A5029297245 @default.
• W2037774992 hasAuthorship W2037774992A5030905729 @default.
• W2037774992 hasAuthorship W2037774992A5031560900 @default.
• W2037774992 hasAuthorship W2037774992A5038542046 @default.
• W2037774992 hasAuthorship W2037774992A5073504542 @default.
• W2037774992 hasAuthorship W2037774992A5086792424 @default.
• W2037774992 hasAuthorship W2037774992A5089537116 @default.
• W2037774992 hasBestOaLocation W20377749921 @default.
• W2037774992 hasConcept C104317684 @default.
• W2037774992 hasConcept C118487528 @default.
• W2037774992 hasConcept C126322002 @default.
• W2037774992 hasConcept C149737253 @default.
• W2037774992 hasConcept C164705383 @default.
• W2037774992 hasConcept C180754005 @default.
• W2037774992 hasConcept C27016395 @default.
• W2037774992 hasConcept C2776268601 @default.
• W2037774992 hasConcept C2780827179 @default.
• W2037774992 hasConcept C2909556870 @default.
• W2037774992 hasConcept C54355233 @default.
• W2037774992 hasConcept C71924100 @default.
• W2037774992 hasConcept C84393581 @default.
• W2037774992 hasConcept C86803240 @default.
• W2037774992 hasConceptScore W2037774992C104317684 @default.
• W2037774992 hasConceptScore W2037774992C118487528 @default.
• W2037774992 hasConceptScore W2037774992C126322002 @default.
• W2037774992 hasConceptScore W2037774992C149737253 @default.
• W2037774992 hasConceptScore W2037774992C164705383 @default.
• W2037774992 hasConceptScore W2037774992C180754005 @default.
• W2037774992 hasConceptScore W2037774992C27016395 @default.
• W2037774992 hasConceptScore W2037774992C2776268601 @default.
• W2037774992 hasConceptScore W2037774992C2780827179 @default.
• W2037774992 hasConceptScore W2037774992C2909556870 @default.
• W2037774992 hasConceptScore W2037774992C54355233 @default.
• W2037774992 hasConceptScore W2037774992C71924100 @default.
• W2037774992 hasConceptScore W2037774992C84393581 @default.
• W2037774992 hasConceptScore W2037774992C86803240 @default.
• W2037774992 hasIssue "3" @default.
• W2037774992 hasLocation W20377749921 @default.
• W2037774992 hasLocation W20377749922 @default.
• W2037774992 hasOpenAccess W2037774992 @default.
• W2037774992 hasPrimaryLocation W20377749921 @default.
• W2037774992 hasRelatedWork W101954376 @default.
• W2037774992 hasRelatedWork W2030129206 @default.
• W2037774992 hasRelatedWork W2147964237 @default.
• W2037774992 hasRelatedWork W2162326163 @default.
• W2037774992 hasRelatedWork W2334275443 @default.
• W2037774992 hasRelatedWork W2365613761 @default.
• W2037774992 hasRelatedWork W2473378103 @default.
• W2037774992 hasRelatedWork W3029310386 @default.
• W2037774992 hasRelatedWork W4311543817 @default.

• next