الفهرس | Only 14 pages are availabe for public view |
Abstract Summary Myocardial infarction (MI), is a multifactorial progressive disease, means that part of the heart muscle suddenly loses its blood supply. Without prompt treatment, this can lead to damage to the affected part of the heart. It sometimes called a heart attack or coronary thrombosis The human SIRT3 gene is localized to the chromosome 11p15.5, and encodes an NAD+ dependent mitochondrial deacetylase of 399-amino acids containing an N-terminal mitochondrial targeting signal and a central catalytic domain . There are many genetic factors contributed to myocardial infarction, one of these is SIRT3 gene promoter polymorphism Myocardial infarction is a complex multifactorial, polygenic disorder which results from the interaction between individual’s genetic makeup and various environmental factors. The principal pathogenesis of MI is the rupture of coronary atherosclerotic plaques. Recent studies have demonstrated the protective roles of SIRT1 in inflammation processes, vascular endothelial homeostasis and atherosclerosis , providing evidence that SIRT1 may play an important role in the pathogenesis of MI. The aim of this study is to determine whether there is a link between SIRT3 promoter variant rs12293349 polymorphisms and SIRT1 rs7069102 and myocardial infarction patients to figure out if they play a role in disease susceptibility. The present study was conducted on seventy subjects: 100 myocardial infarction patients selected from Cardiology Department |