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Abstract
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.
Acknowledgments
The authors thank the Liga Portuguesa contra o Cancro-Centro Regional do Norte (Portuguese League against Cancer), IPO-Porto (CI-IPOP-22-2015 and CI-IPOP-91-2018, Minister of Health of Portugal [CFICS-80/2007]) and Fundação para a Ciência e Tecnologia (FCT).
Financial & competing interests disclosure
J Assis (SFRH/BD/98536/2013) is a grant holder from FCT. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
No writing assistance was utilized in the production of this manuscript.