Platelet Disorders and Treatments
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Latest in Platelet Disorders and Treatments
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Loss of histone readers MLLT1 and MLLT3 eliminates all AID-dependent mutagenic activity, highlighting their essential role in locus-specific antibody diversification.
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CALR-mutated myeloproliferative neoplasms originate mainly from expansion of Vwf-positive, platelet-biased hematopoietic stem cells, with CALRdel52 mutations showing greater amplification.
Fibrocytes are the main collagen-producing cells in JAK2V617F-mutated myelofibrosis, accounting for nearly two-thirds of collagen production in the bone marrow.
- Open access
mRNA-encoded CD19-targeting T cell engager achieves complete B cell depletion and durable platelet recovery in refractory immune thrombocytopenia with minimal safety concerns.
- Open access
Thrombopoietin receptor agonists effectively manage chemotherapy-induced thrombocytopenia, improving patient outcomes in 4 illustrative clinical cases.
The spleen filters activated platelets to prevent thrombosis and inflammation, maintaining systemic platelet quiescence and reducing thrombo-inflammatory risk in mice.
Targeting CXCR7 increases anticoagulant long-chain acylcarnitines in platelets and reduces thrombotic activity, offering a potential therapeutic approach for thrombosis.
P-selectin marks early functional heterogeneity in aging hematopoietic stem cells, with high expression linked to increased DNA damage and myeloid bias in humans and mice.
- Open access
Histidine-rich glycoprotein (HRG) inhibits platelet adhesion and aggregation by binding to GPIbα and GPIIb/IIIa, reducing thrombus formation under high-shear conditions.
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