Miguel Batuecas, AndreaPablo Moreno, Juan Andrés dePorras, NéstorBermejo Álvarez, PabloGonzález Brusi, LeopoldoSerrano, Luis J.Pablo Moreno, Javier María deSánchez, María JoséGarcía Arranz, MarianoRodríguez Bertos, AntonioEt. al.2026-04-072026-04-072026Miguel-Batuecas, A., De Pablo-Moreno, J. A., Porras, N., Bermejo-Álvarez, P., González-Brusi, L., Serrano, L. J., De Pablo-Moreno, J. M., Sánchez, M. J., García-Arranz, M., Rodríguez-Bertos, A., Chumappumkal Joseph, B., Revuelta, L., & Liras, A. (2026). Effect of a truncated mutant factor V on hemostatic function and embryonic development in mice. Scientific Reports, 16(1), 8460. https://doi.org/10.1038/s41598-026-38387-w2045-2322https://hdl.handle.net/11268/17008Factor V is an essential protein in the blood clotting process and plays a central role in secondary hemostasis. Its deficiency causes a rare inherited disorder characterized by episodes of severe bleeding, some of which can be life-threatening. Although previous studies have established that factor V is essential for normal embryonic development, its specific contribution to vascular maturation remains incompletely understood, factor V is believed to contribute to blood vessel stabilization and regulate angiogenesis through its interaction with thrombin. In a recent study, a CRISPR-engineered mouse model intended to produced a mild factor V deficiency disease, unexpectedly produced a frameshift mutation in the A3 domain, resulting in a truncated protein. Factor V levels in healthy embryonic mouse tissues were assessed to investigate its role at different developmental stages. The mutation markedly impaired viability, as homozygous mice exhibited a lethal phenotype with severe bleeding and perinatal death, along with impaired coagulation function. Histopathological and immunohistochemical analyses indicated a link between factor V deficiency, thrombin and α-smooth muscle actin, potentially affecting proangiogenic signaling and embryonic vascular formation. Factor V gene expression increased during late embryogenesis, underscoring its importance in vascular development and maturation. Overall, these findings are consistent with a role for factor V in stabilizing embryonic blood vessels and modulating thrombin-dependent angiogenesis, and add further detail on the developmental impact of its deficiency and the pathogenesis of congenital bleeding disorders.enghttps://creativecommons.org/licenses/by-nc-nd/4.0/Veterinariajournal article10.1038/s41598-026-38387-wopen accessEmbriónInvestigación médicaBiología celularAttribution-NonCommercial-NoDerivatives 4.0 InternationalGoal 3: Ensure healthy lives and promote well-being for all at all ages