Aberrant erythrocyte rigidity in JAK2(V617F) myeloproliferative neoplasms underlies concurrent thrombosis and hemorrhage.

JAK2V617F mutation causes erythrocyte stiffening that impairs clot contraction and promotes unstable thrombi in myeloproliferative neoplasms.

• Why it matters: Understanding how erythrocyte mechanics influence clot formation is crucial because MPN patients experience both thrombosis and hemorrhage, complicating treatment strategies.
• What they did: Researchers used human samples and lineage-specific knockin mice to analyze erythrocyte properties, including biophysical, proteomic, and lipidomic assessments, revealing intrinsic erythrocyte stiffening due to JAK2V617F.
• The result: The mutation-induced rigid erythrocytes impair clot contraction, leading to larger, occlusive, yet unstable thrombi, suggesting that targeting erythrocyte mechanics could offer new therapeutic avenues.