Hutchinson-Gilford progeria syndrome mice display accelerated arterial thrombus formation and increased platelet reactivity

Puspitasari, Yustina M; Ministrini, Stefano; Han, Jiaying; Karch, Caroline; Prisco, Francesco; Liberale, Luca; Bengs, Susan; Akhmedov, Alexander; Montecucco, Fabrizio; Beer, Jürg H; Lüscher, Thomas F; Bongiovanni, Dario; Camici, Giovanni G

doi:10.1016/j.thromres.2024.109100

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Puspitasari, Y. M., Ministrini, S., Han, J., Karch, C., Prisco, F., Liberale, L., Bengs, S., Akhmedov, A., Montecucco, F., Beer, J. H., Lüscher, T. F., Bongiovanni, D., & Camici, G. G. (2024). Hutchinson-Gilford progeria syndrome mice display accelerated arterial thrombus formation and increased platelet reactivity. Thrombosis Research, 241, 109100. https://doi.org/10.1016/j.thromres.2024.109100

Abstract

Introduction: Hutchinson-Gilford Progeria Syndrome (HGPS) is an ultra-rare premature aging genetic disorder caused by a point mutation in the lamin A gene, LMNA. Children with HGPS display short lifespans and typically die due to myocardial infarction or ischemic stroke, both acute cardiovascular events that are tightly linked to arterial thrombosis. Despite this fact, the effect of the classic HGPS LMNA gene mutation on arterial thrombosis remains unknown.

Methods: Heterozygous Lmna$^{G609G}$ knock-in (Lmna$^{G609G/+}$