Unraveling modulators of platelet reactivity in cardiovascular patients using omics strategies: Towards a network biology paradigm

Publication date: 2013 Source:Translational Proteomics, Volume 1, Issue 1 Author(s): Anne Zufferey , Mark Ibberson , Jean-Luc Reny , Ioannis Xenarios , Jean-Charles Sanchez , Pierre Fontana Platelets play an important role in the pathogenesis and the ischemic complications of atherosclerosis. Platelets may be activated by several different agonists, promoting the release of their granule contents and subsequent aggregation and thrombus formation; this leads to ischemic events such as myocardial infarction or stroke. Aspirin, the most popular antiplatelet agent, is a cornerstone in the treatment and prevention of ischemic events in cardiovascular patients. It inhibits a particular amplification pathway of platelet activation, based on thromboxane A2 (TxA2) generation. However, despite a consistent inhibition of TxA2 production, a substantial proportion of patients display preserved platelet function. This phenotype is defined as “high on-treatment platelet reactivity”. It is a risk factor for the recurrence of ischemic events, particularly in acute vessel injury settings. The determinants of platelet reactivity in these patients remain unclear, but previous studies, including healthy subjects, suggested that it is genetically determined. Over the last decade, technological improvements have led to the development of highly efficient omics strategies. High-throughput genomics, transcriptomics and proteomics have the potential to dissect fine metabolic modulations....
Source: Translational Proteomics - Category: Biomedical Science Source Type: research