AI Article Synopsis
- * The deficiency in FVIII is linked to issues like abnormal bone remodeling and inflammation, which can create unusual blood vessel growth.
- * New treatments, like emicizumab, aim to improve blood clotting by bypassing the antibodies that stop FVIII infusions from working, and there is ongoing research into FVIII's additional roles for future therapies.
Article Abstract
Hemophilia A is an X-linked hereditary disorder that results from deficient coagulation factor VIII (FVIII) activity, leading to spontaneous bleeding episodes, particularly in joints and muscles. FVIII deficiency has been associated with altered bone remodeling, dysregulated macrophage polarization, and inflammatory processes that are associated with the neoformation of abnormal blood vessels. Treatment based on FVIII replacement can lead to the development of inhibitors that render FVIII concentrate infusion ineffective. In this context, hemophilia has entered a new therapeutic era with the development of new drugs, such as emicizumab, that seek to restore the hemostatic balance by bypassing pathologically acquired antibodies. We discuss the potential extrahemostatic functions of FVIII that may be crucial for defining future therapies in hemophilia.
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| http://dx.doi.org/10.1016/j.drudis.2021.07.015 | DOI Listing |
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