Chinese scientists reveal the mechanism of immune thrombocytopenia
November 19, 2018 Source: Ministry of Science and Technology
Window._bd_share_config={ "common":{ "bdSnsKey":{ },"bdText":"","bdMini":"2","bdMiniList":false,"bdPic":"","bdStyle":" 0","bdSize":"16"},"share":{ }};with(document)0[(getElementsByTagName('head')[0]||body).appendChild(createElement('script')) .src='http://bdimg.share.baidu.com/static/api/js/share.js?v=89860593.js?cdnversion='+~(-new Date()/36e5)];Recently, the research team of Suzhou University published an online report entitled "Akt-mediated platelet apoptosis and its therapeutic implications in immune thrombocytopenia" in the internationally renowned journal Proceedings of the United States (PNAS). A research paper on the use of thrombocytopenia reveals a new mechanism for the development of immune thrombocytopenia (ITP) and its treatment strategies.
Immune thrombocytopenia (ITP) is a serious threat to human health and can cause death from internal bleeding due to severe thrombocytopenia. For a long time, scholars at home and abroad have been studying ITP. Because its mechanism has not been fully elucidated, some patients still have poor or no response to various existing treatment strategies. ITP patients with anti-platelet glycoprotein (GP) Ib-IX autoantibodies have clinically lower platelet counts and poor response to existing conventional therapies such as hormones, immunoglobulins, and even splenectomy. Studies have shown that anti-GPIb-IX antibodies can lead to platelet Akt activation, Akt is reduced by phosphodiesterase (PDE3A)-regulated protein kinase A (PKA) activity to induce platelet apoptosis, and platelets are activated by the Akt pathway. Apoptotic and activated platelets expose the surface of the membrane to phosphatidylserine (PS), allowing platelets to be recognized by the liver's Coffer cells and phagocytosed. Studies have also found that inhibition of the biological activities of GPIb-IX, PDE3A, PKA, PS, etc., or gene knockout related proteins can inhibit the elimination of platelets caused by antibodies and increase the number of platelets.
This study reveals the mechanism of immune thrombocytopenia and provides a variety of new targets and strategies for the development of drugs for the treatment of thrombocytopenia.
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