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Unraveling modulators of platelet reactivity incardiovascular patients using omics strategies: Towards anetwork biology paradigm

Published inTranslational proteomics, vol. 1, no. 1, p. 25-37
Publication date2013
Abstract

Platelets play an important role in the pathogenesis and the ischemic complications ofatherosclerosis. Platelets may be activated by several different agonists, promoting therelease of their granule contents and subsequent aggregation and thrombus formation; thisleads to ischemic events such as myocardial infarction or stroke. Aspirin, the most popularantiplatelet agent, is a cornerstone in the treatment and prevention of ischemic events incardiovascular patients. It inhibits a particular amplification pathway of platelet activation,based on thromboxane A2 (TxA2) generation. However, despite a consistent inhibition ofTxA2 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 forthe recurrence of ischemic events, particularly in acute vessel injury settings. The determi-nants of platelet reactivity in these patients remain unclear, but previous studies, includinghealthy subjects, suggested that it is genetically determined.

Funding
  • Swiss National Science Foundation - 144150
Citation (ISO format)
ZUFFEREY BAKOS, Anne et al. Unraveling modulators of platelet reactivity incardiovascular patients using omics strategies: Towards anetwork biology paradigm. In: Translational proteomics, 2013, vol. 1, n° 1, p. 25–37. doi: 10.1016/j.trprot.2013.04.002
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ISSN of the journal2212-9626
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Creation09/01/2013 10:13:00 PM
First validation09/01/2013 10:13:00 PM
Update time03/14/2023 8:24:15 PM
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