Abstract
Coronary artery disease (CAD) is a multifactorial disease that involves genetic and environmental interaction. In addition to the well-known CAD risk factors, such as diabetes mellitus, hypertension, hyperlipidemia, and atherosclerosis, it has a genetic component that predisposes to its occurrence even in young people. One of the most commonly studied genes that increase the susceptibility to CAD is renin-angiotensin system (RAS) genes polymorphisms mainly angiotensin-converting enzyme gene (ACE) polymorphisms, angiotensinogen polymorphisms, angiotensin- II type 1 receptor gene polymorphisms, and many other genes. These genetic polymorphisms have a direct association with CAD development or indirect association through causing atherosclerosis and hypertension which, in turn, are complicated by CAD later on. The difference between genetic mutations and polymorphisms lies in the frequency of the abnormal genotype. If the frequency is 1% and more in the general population, it is called polymorphism and if it is less than 1%, then it is called a mutation.According to our findings, after thorough searching, which support the association of RAS genes polymorphisms with premature CAD, hypertension, hypertrophic cardiomyopathy, and atherosclerosis, we recommend additional studies in the form of clinical trials and meta-analyses aiming to create a specific diagnostic tool for CAD risk assessment and discovering the high-risk people as early as possible. Targeted gene therapy, being the future of medicine, needs to be taken into researchers' consideration. It can have promising results in these cases.
Highlights
BackgroundCardiovascular diseases are the leading cause of death and are considered major causes of morbidity and mortality worldwide
Several genetic polymorphisms were studied for their association with Coronary artery disease (CAD) and myocardial infarction (MI) risk, such as factor v Leiden, factor II prothrombin, endothelial nitric oxide synthase, methyltetrahydrofolate reductase (MTHFR), plasminogen activator inhibitor type 1 (PAI-1), paraoxonase (PON-1), APOA5 [4,5,6,7,8]
Genetic susceptibility is a key element in the multifactorial pathogenesis of CAD that should be taken into consideration
Summary
Cardiovascular diseases are the leading cause of death and are considered major causes of morbidity and mortality worldwide. These contradictory results may be attributed to the low sample size It is well-known that CAD is a disease of older adults with risk factors like hypertension, hyperlipidemia, smoking, or diabetes mellitus; studies have shown that ACE DD, ACE ID, and AGT MM genotypes are considered independent risk factors of premature CAD [24,25]. One of them is a missense single-nucleotide change of G to T at position 894 (Glu298Asp) in exon 7 of the gene [4] This polymorphism leads to decreased synthesis and activity of eNOS and nitric oxide; it is considered a risk factor for developing CAD [40]. How can we interfere with these genetic polymorphisms to save those people with genetic predisposition from suffering serious cardiovascular events? And that is where the role of targeted gene therapy comes into play
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