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December 8, 2025Blood

The anti-MPL antibody AMM2 prevents cardiovascular dysfunction in a mouse model of myeloproliferative neoplasms

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Authors

HZHaoyi Zheng

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Overview

Treatment with AMM2 improves cardiac function and reduces lipid-induced cardiovascular issues in myeloproliferative neoplasms.

Key Points

  • Cardiac function improved in JAK2V617F-mutant mice treated with AMM2, maintaining fractional shortening at 37%.
  • At 8 weeks post-transplant, mutant mice exhibited elevated blood cell counts but normal cardiac function on regular diet.
  • Analysis utilized single-cell RNA sequencing to assess changes in cardiac cells under high-fat diet conditions.
  • The findings suggest targeting endothelial function may offer new treatment strategies for cardiovascular diseases linked to MPN.

Cite This Study

Haoyi Zheng (2025) studied this question.

synapsesocial.com/papers/69362f7f4fa91c937236e5afhttps://doi.org/10.1182/blood-2025-5544
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Interleukin-12 and TNFα signaling drives parallel evolution of independent leukemic clones in JAK2V617F mutant myeloproliferative neoplasms2025
  2. 2Single-cell transcriptomic studies reveal altered heterogeneity in CD41 enriched megakaryocytes after targeted therapy in myeloproliferative neoplasm2025
  3. 3PITPβ loss disrupts malignant pAKT activation to ameliorate Jak2 V617F-induced myeloproliferative neoplasms (MPN) in mice2025 · 1 citations
  4. 4HiJAKing the Hematopoietic System: A Low-Frequency JAK2V617F Clone Drives Myeloproliferative Neoplasm Pathology2025 · 3 citations
  5. 5Hematopoietic JAK2V617F mutation increases susceptibility to atrial fibrillation via NLRP3 inflammasome activation in macrophages2025