1403/01/31
اباصلت حسین زاده کلاگر

اباصلت حسین زاده کلاگر

مرتبه علمی: استاد
ارکید:
تحصیلات: دکترای تخصصی
اسکاپوس:
دانشکده: دانشکده علوم پایه
نشانی:
تلفن: 01135302452

مشخصات پژوهش

عنوان
Human AGT-p.Met268Thr and coronary heart disease risk: a case-control study and meta-analysis.
نوع پژوهش
JournalPaper
کلیدواژه‌ها
coronary disease, angiotensinogen, genetc polymorphism, meta-analysis.
سال
2018
مجله Family Medicine and Primary Care Review
شناسه DOI
پژوهشگران Hanieh Mohammadi ، Narges Razavi ، Ali Abbasi ، Faezeh Babaei ، Ensiyeh Seyedrezazadeh ، Abasalt Hosseinzadeh Colagar

چکیده

Background. Polymorphisms in genes, which is involved in the renin–angiotensin system, play an important role in the pathogenesis of coronary heart disease (CHd). Polymorphism of c.803t>C in the human angiotensinogen gene results in methionine(M) to threonine (T) substtuton at codon 268 (p.Met268Thr), which traditonally has been known as M235T. This polymorphism may contribute to cardiovascular diseases. Objectves. The aim of this study was to investgate the associaton between p.Met268Thr polymorphism in the angiotensinogen gene and coronary heart disease (CHd) through a case-control study, which is followed by a meta-analysis. Material and methods. In the case-control study, c.803T>C genotyping of 217 subjects (102 CHD cases vs 115 controls) was investgated by the polymerase chain reacton-restricton fragment length polymorphism (PCR-RFLP) method. In the meta-analysis, 31 studies were included, reflectng 12,028 people with CHD and 16,362 healthy controls. Results. The data from the case-control study revealed that MT (OR, 1.875; 95%CI, 1.060–3.316; p = 0.031) and TT (OR, 3.389; 95%CI, 1.251–9.179; p = 0.016) genotypes are signifcantly associated with CHD. The meta-analysis revealed a signifcant associaton in the recessive model (OR, 1.156; 95%CI, 1.011–1.321; p = 0.034). Conclusions. Although the pooled OR of the meta-analysis showed that there is an increased risk of CHD conferred by p.Met268Thr of the AGT gene, this associaton was weak, which could be atributed to a bias in publicatons.