Why the study?
CYP2A6 is highly polymorphic and metabolizes nicotine, a major risk factor for cardiovascular disease, but the effects of its polymorphisms on cardiovascular diseases required evaluation.
Does CYP2A6 gene polymorphism affect the risk of cardiovascular diseases in active or passive smokers?
Does CYP2A6 gene polymorphism affect the risk of cardiovascular diseases in active or passive smokers?
CYP2A6 gene polymorphisms that cause slow nicotine metabolism increase the risk of atherosclerosis and cardiovascular diseases in individuals exposed to nicotine.
CYP2A6 variants may modulate nicotine-related CV risk; leaves open whether genotyping aids risk stratification or cessation.
The CYP2A6 gene encodes its enzymes and is highly polymorphic, leading to variations in allele forms, both in the active and inactive states. These changes result in a decrease, increase or deletion of enzyme activities. One of the specific substrates is nicotine, an active compound in cigarettes. Nicotine is a major risk factor for cardiovascular diseases, and the inactive alleles tends to decrease its metabolism and expands the threat to infections. Therefore, this study aims to evaluate the effects of CYP2A6gene polymorphism on cardiovascular diseases. Relevant literatures were obtained using PubMed and Google Scholar, while the eventual selection followed the inclusion and exclusion criteria. Based on this review, the CYP2A6 gene polymorphism, both in increased, decreased or deleted alleles, was known to significantly influence nicotine metabolism and its blood levels. Species categorized as slow or poor metabolizers, tend to decrease the nicotine metabolism, but result in greater nicotine blood levels. This outcome subsequently accelerated the activation of the sympathetic nervous system, lipolysis, and insulin resistance, to trigger atherosclerosis. In summary, CYP2A6 gene polymorphism is known to increase cardiovascular diseases, particularly among active or passive smokers.
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Prasojo et al. (2021) studied this question.
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