Key result
Genetic factors, particularly SNPs in cyclooxygenase, thromboxane, and platelet receptor-related genes, appear to play a preponderant role in the multifactorial etiology of aspirin resistance.
Why the study?
Although aspirin resistance is frequently observed and genetic factors appear preponderant, this complex process remains poorly understood.
Genetic factors, particularly SNPs in cyclooxygenase, thromboxane, and platelet receptor genes, are key contributors to aspirin resistance and may serve as predictive biomarkers.
Variants in cyclooxygenase and platelet pathways may associate with aspirin resistance; leaves open pharmacogenomic personalization of antiplatelet therapy.
Despite the clinical benefits of aspirin, the interindividual variation in response to this antiplatelet drug is considerable. The manifestation of aspirin resistance (AR) is frequently observed, although this complex process remains poorly understood. While AR etiology is likely to be multifactorial, genetic factors appear to be preponderant. According to several genetic association studies, both genome-wide and candidate gene studies, numerous SNPs in cyclooxygenase, thromboxane and platelet receptors-related genes have been identified as capable of negatively affecting aspirin action. Thus, it is essential to understand the clinical relevance of AR-related SNPs as potential predictive and prognostic biomarkers as they may be essential to defining the AR phenotype.
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Ferreira et al. (2020) conducted a review in Aspirin resistance. SNPs in cyclooxygenase, thromboxane and platelet receptors-related genes was evaluated. Genetic factors, particularly SNPs in cyclooxygenase, thromboxane, and platelet receptor-related genes, appear to play a preponderant role in the multifactorial etiology of aspirin resistance.
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