María Villa-Fajardo
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
María Villa-Fajardo has a total of 10 co-authors. Here are the top co-authors by number of shared publications:
- Andrea Acebes-Huerta
Platelet Research Lab, Instituto de Investigación Sanitaria del Principado de Asturias (ISPA), 33011 Oviedo, Spain
1 shared publication - Dick H. W. Dekkers
Proteomics Center, Erasmus University Medical Center, Rotterdam, The Netherlands
1 shared publication - Graciela Carbajo-Argüelles
Platelet Research Lab, Instituto de Investigación Sanitaria del Principado de Asturias (ISPA), 33011 Oviedo, Spain
1 shared publication - Iris Maria De Cuyper
Sanquin Blood Supply Foundation, Department Research, Amsterdam, The Netherlands
1 shared publication - Jaap Jan Zwaginga
Department of Hematology, Leiden University Medical Center, Leiden, The Netherlands
1 shared publication - Jean-Louis H. Kerkhoffs
Department of Hematology HagaZiekenhuis The Hague the Netherlands
1 shared publication
Latest Publications
- Open Access
- 22 May 2026
- Published by MDPI AG in Biomolecules
- Vol. 16 (6) , 761
The Plasma Glycoprotein Milieu in the Hemato-Oncological Patient Inhibits Platelet Function
Hemato-oncological patients with chemotherapy-induced thrombocytopenia are a major recipient group of frequent platelet (PLT) transfusion. Prophylactic platelet transfusions are administered when platelet counts fall below 10 × 109 PLT/L, to prevent severe or fatal bleeding. However, these prophylactic platelet transfusions do not always result in the prevention of bleeding. Pre- or post-transfusion acquired dysfunction of donor platelets in this respect could play a role. We previously reported intrinsic and transfusion-dependent platelet alterations in hemato-oncological patients. In particular, the expression of relevant platelet receptors was affected in donor platelets after incubation with patient’s plasma, which could explain, at least in part, the variable efficacy of platelet transfusions in these patients. In the present manuscript we show that plasma from acute myeloid leukemia (AML) patients undergoing chemotherapy inhibits functionality of allogenic platelets. Further proteomic analysis allowed us to observe alterations in the composition of plasma samples, and to identify key plasma components which could be responsible for platelet function inhibition and explain bleeding in patients notwithstanding platelet transfusions. We anticipate that with the obtained results, platelet transfusion support can be further personalized in patients receiving chemotherapy and applications might expand to maximize the clinical efficacy of procedures such as bone marrow transplantation.
- 22 May 2026
- Published by MDPI AG in Biomolecules
- Vol. 16 (6) , 761
Open AccessThe Plasma Glycoprotein Milieu in the Hemato-Oncological Patient Inhibits Platelet Function
Hemato-oncological patients with chemotherapy-induced thrombocytopenia are a major recipient group of frequent platelet (PLT) transfusion. Prophylactic platelet transfusions are administered when platelet counts fall below 10 × 109 PLT/L, to prevent severe or fatal bleeding. However, these prophylactic platelet transfusions do not always result in the prevention of bleeding. Pre- or post-transfusion acquired dysfunction of donor platelets in this respect could play a role. We previously reported intrinsic and transfusion-dependent platelet alterations in hemato-oncological patients. In particular, the expression of relevant platelet receptors was affected in donor platelets after incubation with patient’s plasma, which could explain, at least in part, the variable efficacy of platelet transfusions in these patients. In the present manuscript we show that plasma from acute myeloid leukemia (AML) patients undergoing chemotherapy inhibits functionality of allogenic platelets. Further proteomic analysis allowed us to observe alterations in the composition of plasma samples, and to identify key plasma components which could be responsible for platelet function inhibition and explain bleeding in patients notwithstanding platelet transfusions. We anticipate that with the obtained results, platelet transfusion support can be further personalized in patients receiving chemotherapy and applications might expand to maximize the clinical efficacy of procedures such as bone marrow transplantation.