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Antiplatelet drugs are one of the main tools used to prevent thrombus formation in people who have had a heart attack or stroke or who have cardiovascular diseases with a high thrombotic risk. These treatments work by reducing platelets’ ability to aggregate and form clots that can obstruct the arteries. However, their use also increases the risk of bleeding, a common complication that limits their use in certain patients and remains one of the major challenges in cardiology today.
Now, a study by researchers from the Sant Pau Research Institute (IR Sant Pau) and the Centro de Investigación Biomédica en Red de Enfermedades Cardiovasculares (CIBERCV) identifies a new protein involved in platelet activation that could help advance toward safer antithrombotic therapies. The work, published in the journal European Heart Journal, shows for the first time that the LRP5 protein, known for its role in the WNT signaling pathway, is directly involved in platelet aggregation and in arterial thrombus formation. The relevance of the finding led the same journal to simultaneously publish an independent editorial on new antithrombotic strategies capable of reducing bleeding risk.
“We have observed that both the genetic deletion of LRP5 and its pharmacological inhibition very significantly reduce platelet activation and thrombus formation in preclinical models, but with a much lower bleeding impact than that of classic antiplatelet agents such as aspirin or clopidogrel,” highlights Dr. Maria Borrell-Pages, researcher in the Molecular Pathology and Therapeutics of Atherothrombotic and Ischemic Diseases group at IR Sant Pau and CIBERCV and corresponding author of the study.
