Exploring the Interplay: Aspirin Therapy, Genetic Polymorphisms, and Homocysteine Levels in Cardiovascular Disease Patients. International Journal of Pharmaceuticals, Nutraceuticals and Cosmetic Science, 7 (2). pp. 1-10. ISSN 2682-8146 (2024)
Abstract
Cardiovascular disease (CVD) is a significant worldwide health threat expected to cause 23.6 million deaths
annually by 2030. Homocysteine is an amino acid that is generated during the breakdown of methionine.
Elevated levels of homocysteine are recognised as a standalone risk factor for cardiovascular disease, such as
coronary artery disease and stroke. Methylenetetrahydrofolate reductase (MTHFR) and methionine synthase
(MS) play essential roles in regulating homocysteine levels and maintaining cardiovascular health. The C677T
(rs1801133) mutation of the MTHFR gene is closely linked to coronary artery disease due to decreased enzyme
activity while the A2756G mutation (rs1805087) in the MS gene disrupts the remethylation process and is
linked to elevated homocysteine levels and a higher risk of cardiovascular disease. Aspirin is a key treatment
for cardiovascular disease by preventing platelet activation and aggregation, reducing the likelihood of blood
clot formation. In addition, aspirin usage seems to be connected to homocysteine levels in persons dealing with
CVD. The precise interplay between aspirin therapy, genetic polymorphisms, and their collective impact on
homocysteine levels in CVD patients remains unclear. Therefore, this investigation aims to explore the effects
of genetic polymorphisms (MTHFR and MS genes) and aspirin therapy on homocysteine levels in CVD
patients from two hospitals in Selangor, Malaysia. Blood samples from 52 patients were collected and analysed,
with homocysteine levels quantified using LCMS-QQQ, aspirin abundance determined through LCMS-QTOF,
and genetic polymorphisms of MTHFR and MS genes identified using RT-PCR. Interestingly, individuals with
CVD exhibiting elevated homocysteine levels did not show the mutant genotype for neither MTHFR nor MS
genes. Furthermore, the potential influence of aspirin therapy emerged as a plausible explanation for the
observed lower homocysteine levels in these patients. Other variables than genetic predisposition may play a
role in causing elevated homocysteine levels in people with CVD. Our findings suggest that aspirin therapy
may have a potential impact on reducing homocysteine levels in these patients. However, more research is
needed to understand the underlying mechanisms.
| Item Type: | Article |
|---|---|
| Keywords: | Cardiovascular Disease, Homocysteine, Aspirin, Methylenetetrahydrofolate Reductase, Methionine Synthase |
| Taxonomy: | By Niche > Genome > Bacterial Genomes By Niche > Genome > Genomes Data Processing By Niche > Genome > Human Genome |
| Local Content Hub: | Niche > Genome |
| Depositing User: | Hazrul Amir Tomyang (Puncak Alam) |
| Date Deposited: | 12 Mar 2025 08:33 |
| Last Modified: | 12 Mar 2025 08:33 |
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