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Vasoreparative processes in the pathogenesis of deep vein thrombosis (DVT)


About 30% of patients with deep vein thrombosis (DVT) do not present the classic risk factors associated with the onset of the disease, and the molecular mechanisms of DVT remain unclear. Therefore, there is a clear need to investigate new biomarkers that may be associated with this disease, as well as new studies to elucidate the mechanisms that lead to pathogenesis. According to Virchow's triad, endothelial dysfunction may be described as one of the causes, but it is not known whether it may also be a consequence of the disease. It is described so far that such dysfunction has been associated with DVT complications, including post-thrombotic syndrome and recurrence. While extensive research has investigated endothelial damage as a cause of vascular disease, recent studies suggest that vascular repair mechanisms are important. Endothelial progenitor cells appear as new tools to study and treat vascular diseases, but in the context of DVT, little is known and has been researched, as these cells are difficult to obtain. Thus, the SPRINT proposal emerges as a possibility of establishing a partnership that will allow robust investigations in the context presented, given that the Hemostasis laboratory (Hemocenter - UNICAMP) has easier access to samples of patients with DVT and Professor Reinhold Medina. (Queen's University of Belfast) and her lab have expertise in progenitor endothelial cells and vascular biology. (AU)

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