Dimethyl fumarate inhibits antibody-induced platelet destruction in immune thrombocytopenia mouse.

Background: Immune thrombocytopenia (ITP) is an autoimmune disease characterized as a low platelet count resulting from immune-mediated platelet destruction. Dimethyl fumarate (DMF) is widely applied for the treatment of several autoimmune diseases with immunosuppressive effect. However, whether it ameliorates ITP is unclear.

Tacrolimus ameliorates thrombocytopenia in an ITP mouse model.

Immune thrombocytopenia (ITP) is an autoimmune disease characterized by lower platelet count resulting from immune cells-mediated platelet clearance. Tacrolimus is an immunosuppressive agent which selectively inhibits T cell activation. Whether tacrolimus plays a role in ITP remains unclear.

p47phox deficiency impairs platelet function and protects mice against arterial and venous thrombosis.

NADPH oxidase-derived reactive oxygen species (ROS) regulates platelet function and thrombosis. It remains controversial regarding NOX2's role in platelet function. As a regulatory subunit for NOX2, whether p47phox regulates platelet function remains unclear.

Salidroside inhibits platelet function and thrombus formation through AKT/GSK3β signaling pathway.

Salidroside is the main bioactive component in and possesses multiple biological and pharmacological properties. However, whether salidroside affects platelet function remains unclear. Our study aims to investigate salidroside's effect on platelet function.

Thalidomide prevents antibody-mediated immune thrombocytopenia in mice.

Immune thrombocytopenia (ITP) is a heterogeneous autoimmune disorder characterized by immune-mediated platelet destruction, leading to lower platelet count. Thalidomide is considered as a novel immunomodulatory drug for treating several autoimmune diseases. Whether thalidomide can ameliorate ITP remains unclear.

All-Trans Retinoic Acid Impairs Platelet Function and Thrombus Formation and Inhibits Protein Kinase CßI/δ Phosphorylation.

All-trans retinoic acid (ATRA) is widely used for induction of complete remission in patients with acute promyelocytic leukemia (APL). ATRA also regulates protein kinase C (PKC) activity. Therapeutic use of ATRA reportedly interferes with hemostatic function in APL patients, including effects on coagulation or other vascular cells, although effects of ATRA on platelets remain unclear.

Increased GPIbα shedding from platelets treated with immune thrombocytopenia plasma.

Immune thrombocytopenia (ITP) is a heterogeneous autoimmune disease, characterized by accelerated platelet destruction/clearance or decreased platelet production. ADAM17-mediated platelet receptor GPIbα extracellular domain shedding has been shown to be involved in platelet clearance. Whether GPIbα shedding participates in the pathogenesis of ITP remains poorly understood.