Gene Polymorphisms of the Renin-Angiotensin-Aldosterone System as Risk Factors for the Development of In-Stent Restenosis in Patients with Stable Coronary Artery Disease

Азова, М. М.; Timizheva, K. B.; Aissa, A. Ait; Благонравов, М. Л.; Gigani, O. O.; Aghajanyan, Anna; Цховребова, Л. В.

doi:10.3390/biom11050763

Cited by 17 publications

(7 citation statements)

References 39 publications

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“…Our nding was in agreement with that of (Azova et al 2021), who found that the increased frequency of the D allele and DD genotype and decreased frequency of the I allele and ID genotype were found in CAD patients compared to healthy subjects (P = 0.004). Our study was supported by another study by Abdel-Aziz et al (2014), who observed that the ACE DD genotype and D allele were associated with ESRD as risk factors for ESRD in the Egyptian population, while the distribution of the ACE ID genotype and I allele frequency were signi cantly decreased.…”

Section: Resultssupporting

confidence: 93%

Association of Angiotensin-I-Converting Enzyme (ACE) Insertion/ Deletion Gene Polymorphism with Preeclampsia Susceptibility in Egyptian women

Azab

El-kader

Ali

et al. 2023

Preprint

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The current study was designed to investigate the association of angiotensin-I-converting enzyme (I / D) gene polymorphisms with the susceptibility and clinical pattern of preeclampsia among Egyptian cases from the Nile Delta region. Oxidative stress biomarkers, including Serum levels of malondialdehyde, glutathione-s-transferase, superoxide dismutase, nitric oxide, glutathione peroxidase, endothelin-1, and interleukin-6 as a pro-inflammatory biomarker, were assessed by Elisa. In this study, genotyping, and allelic frequencies of the ACE I/D (rs4646994) variant with preeclampsia susceptibility was about 38.2%. In addition, the results revealed that the ACE/ID (rs4646994) genotype distribution was associated with preeclampsia in the studied population from the Nile Delta region of Egypt. Frequencies of the D allele and DD genotype were significantly increased, while frequencies of the I allele and ID genotype were significantly decreased in the preeclampsia patients when compared with the control subjects (P = 0.014, OR = 1.94, 95% CI = 1.254–3.233 for DD) and (P = 0.016, OR = 1.4, 95% CI = 1.061-2.10 for D). Our findings suggest the association between rs4646994 and susceptibility to preeclampsia in Egyptian cases from the Nile Delta region. Examining the impact of ACE gene variants on preeclampsia may be a valuable method for locating and treating women at risk. Moreover, the angiotensin-I-converting enzyme DD genotype and D allele were associated with preeclampsia as risk factors for Egyptian women. There was a significant association between the serum levels of oxidative stress biomarkers and pro-inflammatory biomarker of preeclampsia compared to the healthy group, with P < 0.05.

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Section: Resultssupporting

confidence: 93%

Association of Angiotensin-I-Converting Enzyme (ACE) Insertion/ Deletion Gene Polymorphism with Preeclampsia Susceptibility in Egyptian women

Azab

El-kader

Ali

et al. 2023

Preprint

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“…In our study, the minor allele frequency of these SNPs were comparable to previous reports in Thai, 25 and Chinese 26 populations, but lower than those found in European populations. 27 We found that the variant alleles T (for AGT rs699) and C (for AGTR1 rs5186) were associated with higher BMI, HbA1C and TG levels compared with the wild-type alleles. The interaction between obesity, activation of the RAS, and hypertension has been mentioned in several experimental studies.…”

Section: Discussionmentioning

confidence: 72%

Effects of AGT and AGTR1 Genetic Polymorphisms and Changes in Blood Pressure Over a Five-Year Follow-Up

Chaimati,

Shantavasinkul,

Sritara

et al. 2023

RMHP

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Purpose The renin–angiotensin system plays an important role in the central regulation of blood pressure (BP). Genetic variations of angiotensinogen (AGT) and angiotensin II type 1 receptor (AGTR1) may increase susceptibility to elevated BP and hypertension. This study investigated the effects of AGT rs699 and AGTR1 rs5186 single nucleotide polymorphisms (SNPs) on BP at baseline and at a 5-year follow-up. Paticipants and Methods The study population consisted of participants from the Electricity Generating Authority of Thailand cohort study (n=354); data were collected at baseline (2013) and 5 years later (2018). Genotyping of the two SNPs was performed using TaqMan ® assay and statistical analyses were performed with SNPStats software. Results The frequencies of the two SNPs were within the Hardy–Weinberg equilibrium (p=0.22 for AGT rs699 and p=0.06 for AGTR1 rs5186). For each SNP, mutant genotypes were significantly associated with increased systolic BP and/or diastolic BP in the codominant and recessive models. Risk alleles of AGT rs699 and AGTR1 rs5186 were associated with increased odds of hypertension and hypertension with metabolic syndrome at follow-up. Conclusion Overall, our results suggest that polymorphisms of genes in the renin–angiotensin system increase susceptibility to the development and progression of hypertension and the development of the metabolic syndrome.

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“…These include polymorphisms in the genes of the haemostatic system such as Platelet glycoprotein IIIa and the P2Y 12 receptor. 11 Interestingly, resistance to the drugs eluted from stents seems to occur in genetically predisposed patients as well. 11 …”

Section: Predisposing Factors For In-stent Restenosismentioning

confidence: 99%

In-stent restenosis after percutaneous coronary intervention: emerging knowledge on biological pathways

Pelliccia,

Zimarino,

Niccoli

et al. 2023

European Heart Journal Open

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Percutaneous coronary intervention (PCI) has evolved significantly over the past four decades. Since its inception, in-stent restenosis (ISR) – the progressive reduction in vessel lumen diameter after PCI – has emerged as the main complication of the procedure. Although the incidence of ISR has reduced from 30% at 6 months with bare-metal stents (BMS) to 7% at 4 years with drug-eluting stents (DES), its occurrence is relevant in absolute terms because of the dimensions of the population treated with PCI. The aim of this review is to summarize the emerging understanding of the biological pathways that underlie ISR. ISR is associated with several factors, including patient-related, genetic, anatomic, stent, lesion and procedural characteristics. Regardless of associated factors, there are common pathophysiologic pathways involving molecular phenomena triggered by the mechanical trauma caused by PCI. Such biologic pathways are responses to the denudation of the intima during balloon angioplasty and involve inflammation, hypersensitivity reactions, and stem cell mobilization in particular of endothelial progenitor cells (EPCs). The results of these processes are either vessel wall healing or neointimal hyperplasia and/or neoatherosclerosis. Unraveling the key molecular and signal pathways involved in ISR is crucial to identify appropriate therapeutic strategies aimed at abolishing the ‘Achille’s heel’ of PCI. With this regard, we discuss novel approaches to prevent DES restenosis. Indeed, available evidence suggests that EPCs-capturing stents promote a rapid stent re-endothelisation, which in turn has the potential to decrease the risk of stent thrombosis and allow the use of a shorter duration of dual antiplatelet therapy.

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Gene Polymorphisms of the Renin-Angiotensin-Aldosterone System as Risk Factors for the Development of In-Stent Restenosis in Patients with Stable Coronary Artery Disease

Cited by 17 publications

References 39 publications

Association of Angiotensin-I-Converting Enzyme (ACE) Insertion/ Deletion Gene Polymorphism with Preeclampsia Susceptibility in Egyptian women

Association of Angiotensin-I-Converting Enzyme (ACE) Insertion/ Deletion Gene Polymorphism with Preeclampsia Susceptibility in Egyptian women

Effects of AGT and AGTR1 Genetic Polymorphisms and Changes in Blood Pressure Over a Five-Year Follow-Up

In-stent restenosis after percutaneous coronary intervention: emerging knowledge on biological pathways

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