Renin–angiotensin system genetic polymorphisms: Lack of association with CRP levels in patients with coronary artery disease

Bahramali, Ehsan; Firouzabadi, Negar; Jonaidi-Jafari, Nematollah; Shafiei, Massoumeh

doi:10.1177/1470320312474051

Cited by 12 publications

(7 citation statements)

References 63 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“… 26 A recent study identified the lack of association between six different genetic polymorphisms ( ACE (I/D), A-240T and A2350G, angiotensinogen M235T, AT1 receptor A1166C, and AT2 receptor C3123A polymorphisms) of RAS with increase in serum CRP level. 27 These reports provide evidence that supports the present findings.…”

Section: Discussionsupporting

confidence: 90%

Association of serum levels of AngII, KLK1, andACE/KLK1polymorphisms with acute myocardial infarction induced by coronary artery stenosis

Dai

Feng

et al. 2016

J Renin Angiotensin Aldosterone Syst

View full text Add to dashboard Cite

Introduction:The study aims to confirm the association of acute myocardial infarction (AMI) with serum angiotensin II (AngII), kallikrein1 (KLK1), and ACE/KLK1 polymorphisms.Materials and methods:Serum AngII/KLK1 levels and ACE and KLK1 genotypes were determined in 208 patients with AMI and 216 normal controls. Binary logistic regression was used for data analysis.Results:The differences in serum AngII levels were statistically significant between the groups. After adjusting for potential confounding factors, high serum levels of AngII and KLK1 significantly increased the risk of AMI. The individuals with ACE DD and KLK1 GG genotypes significantly increased the risk of AMI compared with those harboring the ACE II and KLK1 AA genotypes (OR = 8.77, 95% CI = 1.74–44.16).Conclusions:(1) Increasing the serum levels of AngII increased the risk of AMI. (2) The risk of AMI increased significantly when the serum levels of AngII and KLK1 simultaneously increased. (3) Individuals with the combined genotypes of ACE DD and KLK1 GG showed significantly increased risk of AMI compared with those with the combined genotypes of ACE II and KLK1 AA.

show abstract

Section: Discussionsupporting

confidence: 90%

Association of serum levels of AngII, KLK1, andACE/KLK1polymorphisms with acute myocardial infarction induced by coronary artery stenosis

Dai

Feng

et al. 2016

J Renin Angiotensin Aldosterone Syst

View full text Add to dashboard Cite

show abstract

“…Bahramali and co-workers studied this relation in patients with coronary artery disease and they did not find any evidence of an association between this ACE polymorphism and CRP levels. 25 In another study, this relation was tested in patients suffering from advanced cancers. 26 In this study population a trend towards higher CRP levels in carriers of the ACE intron D allele was found, however, without reaching statistical significance.…”

Section: Discussionmentioning

confidence: 99%

Angiotensin converting enzyme intron 16 insertion/deletion genotype is associated with plasma C-reactive protein concentration in uteroplacental dysfunction

Häupl

Zimmermann

Kalus

et al. 2014

J Renin Angiotensin Aldosterone Syst

View full text Add to dashboard Cite

Introduction: Disturbance of the uteroplacental circulation (UPC) and the renin-angiotensin system are involved in the pathogenesis of preeclampsia. In women with history of preeclampsia persistently elevated C-reactive protein (CRP) levels have been described. The angiotensin-converting enzyme (ACE) intron 16 insertion/deletion (I/D) genotype is associated with ACE activity and assumed to be a risk factor for preeclampsia. As ACE generates proinflammatory angiotensin II, we analysed, whether ACE intron 16 I/D genotype is associated with CRP and whether this association exhibited a relation to uteroplacental dysfunction. Materials and methods: A total of 639 women have been followed during pregnancy with repeated measurements of CRP levels (observations: n=2333). ACE intron 16 I/D genotype was determined, and its association with CRP was assessed with adjustment for non-independent observations. Results: CRP levels of ACE D allele carriers were significantly higher than those of the ACE II (wild-type) genotype (p=0.0003, p adj =0.04). This relation was allele-dose dependent (p<10 −4 , p adj <0.02). Association between ACE I/D and CRP was significantly restricted to patients presenting with impaired UPC in univariate (p<0.04) and multivariate analyses (p=0.01). Conclusions:The ACE I/D genotype is significantly associated with CRP elevations during pregnancies complicated by disturbed UPC. Whether this effect on CRP is involved in pathogenesis of preeclampsia has to be elucidated.

show abstract

“…Several studies have shown that non-Hispanic Black (NHB) individuals experience higher rates of symptomatic and radiographic OA, higher age-related average pain intensity, and higher levels of disability than their non-Hispanic White (NHW) counterparts, in addition to higher pain sensitivity [6][7][8]. The role of genetics in various illnesses has been well documented [9][10][11][12][13]. In addition, role of genetics in OA has been supported by many studies, predominantly the single nucleotide polymorphisms (SNPs).…”

Section: Introductionmentioning

confidence: 99%

Metformin attenuates symptoms of osteoarthritis: role of genetic diversity of Bcl2 and CXCL16 in OA

et al. 2023

Self Cite

View full text Add to dashboard Cite

Objective This study aimed to evaluate the effectiveness of metformin versus placebo in overweight patients with knee osteoarthritis (OA). In addition, to assess the effects of inflammatory mediators and apoptotic proteins in the pathogenesis of OA, the genetic polymorphisms of two genes, one related to apoptosis (rs2279115 of Bcl-2) and the other related to inflammation (rs2277680 of CXCL-16), were investigated. Methods In this double-blind placebo-controlled clinical trial, patients were randomly divided to two groups, one group receiving metformin (n = 44) and the other one receiving an identical inert placebo (n = 44) for 4 consecutive months (starting dose 0.5 g/day for the first week, increase to 1 g/day for the second week, and further increase to 1.5 g/day for the remaining period). Another group of healthy individuals (n = 92) with no history and diagnosis of OA were included in this study in order to evaluate the role of genetics in OA. The outcome of treatment regimen was evaluated using the Knee Injury and Osteoarthritis Outcome Score (KOOS) questionnaire. The frequency of variants of rs2277680 (A181V) and rs2279115 (938C>A) were determined in extracted DNAs using PCR-RFLP method. Results Our results indicated an increase in scores of pain (P ≤ 0.0001), activity of daily living (ADL) (P ≤ 0.0001), sport and recreation (Sport/Rec) (P ≤ 0.0001), and quality of life (QOL) (P = 0.003) and total scores of the KOOS questionnaire in the metformin group compared to the placebo group. Susceptibility to OA was associated with age, gender, family history, CC genotype of 938C>A (Pa = 0.001; OR = 5.2; 95% CI = 2.0–13.7), and GG+GA genotypes of A181V (Pa = 0.04; OR = 2.1; 95% CI = 1.1–10.5). The C allele of 938C>A (Pa = 0.04; OR = 2.2; 95% CI = 1.1–9.8) and G allele of A181V (Pa = 0.02; OR = 2.2; 95% CI = 1.1–4.8) were also associated with OA. Conclusion Our findings support the possible beneficial effects of metformin on improving pain, ADL, Sport/Rec, and QOL in OA patients. Our findings support the association between the CC genotype of Bcl-2 and GG+GA genotypes of CXCL-16 and OA.

show abstract

Renin–angiotensin system genetic polymorphisms: Lack of association with CRP levels in patients with coronary artery disease

Cited by 12 publications

References 63 publications

Association of serum levels of AngII, KLK1, andACE/KLK1polymorphisms with acute myocardial infarction induced by coronary artery stenosis

Association of serum levels of AngII, KLK1, andACE/KLK1polymorphisms with acute myocardial infarction induced by coronary artery stenosis

Angiotensin converting enzyme intron 16 insertion/deletion genotype is associated with plasma C-reactive protein concentration in uteroplacental dysfunction

Metformin attenuates symptoms of osteoarthritis: role of genetic diversity of Bcl2 and CXCL16 in OA

Contact Info

Product

Resources

About