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Review
. 2024 Feb;52(2):3000605241230429.
doi: 10.1177/03000605241230429.

Epoxidase inhibitor-aspirin resistance and the relationship with genetic polymorphisms: a review

Xiaolin Hou  1
Affiliations
Review

Epoxidase inhibitor-aspirin resistance and the relationship with genetic polymorphisms: a review

Xiaolin Hou. J Int Med Res. 2024 Feb.

Abstract

Strokes are the leading cause of death in most regions of the world. Epoxidase inhibitors include the drug aspirin (acetylsalicylic acid). Aspirin is widely used as first-line treatment for the prevention of cardiovascular and cerebrovascular diseases in at-risk patients. However, patients using conventional doses of aspirin can still develop ischaemic cardiovascular and cerebrovascular diseases, a phenomenon known as aspirin resistance. The occurrence of aspirin resistance hinders the prevention and treatment of ischaemic cardiovascular and cerebrovascular diseases. There are many factors affecting aspirin resistance, such as sex, drug dose, metabolic disease, genetic polymorphisms, drug interactions and pharmacokinetics. Genetic polymorphism refers to the simultaneous and frequent presence of two or more discontinuous variants or genotypes or alleles in a population of organisms. Platelets contain a large number of highly polymorphic transmembrane glycoprotein receptors encoded by two or more isomeric alleles. Changes in gene polymorphisms in various pathways during platelet aggregation can lead to aspirin resistance. This narrative review describes the gene polymorphisms that have been demonstrated to be significantly associated with aspirin resistance. Research on the mechanisms of aspirin resistance and increased knowledge should provide accurate drug guidance in individuals that require first-line antiplatelet therapy.

Keywords: Aspirin resistance; cyclooxygenase gene; epoxidase inhibitor; gene polymorphism; platelet endothelial aggregation receptor 1 gene; platelet membrane glycoprotein gene.

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Conflict of interest statement

Declaration of conflicting interestThe author declares that there are no conflicts of interest.

Figures

Figure 1.
Figure 1.
Molecular structure of aspirin.
Figure 2.
Figure 2.
Mechanisms of action of aspirin in terms of reducing platelet aggregation. PGG2, prostaglandin G2; PGH2, prostaglandin H2; PG12, prostaglandin I2; TXA2, thromboxane A2; cAMP, cyclic adenosine monophosphate. The colour version of this figure is available at: http://imr.sagepub.com.
See this image and copyright information in PMC

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