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Antithrombotic endothelial dysfunction is prevented by Tie2 activation in severe COVID-19

Antithrombotic endothelial dysfunction is prevented by Tie2 activation in severe COVID-19 Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the novel virus responsible for the ongoing coronavirus disease (COVID-19) pandemic. COVID-19 can cause critical illness characterized by severe pulmonary and extrapulmonary manifestations. The risk of mortality for patients with severe COVID-19 is high. Critical COVID-19 is characterized by thrombotic coagulopathy. Increased levels of D-dimer and activation of coagulation are associated with worse clinical outcomes. Fibrin deposition is common in the lung vasculature in chronic COVID-19. Research suggests that COVID-19 pathophysiology may be affected by microvascular thrombosis. Severe COVID-19 may be associated with increased circulating levels of several biomarkers

Scientists discovery of blood clotting mechanism could lead to new antithrombotic drugs

 E-Mail Under normal, healthy circulatory conditions, the von Willebrand Factor (vWF) keeps to itself. The large and mysterious glycoprotein moves through the blood, balled up tightly, its reaction sites unexposed. But when significant bleeding occurs, it springs into action, initiating the clotting process. When it works properly, vWF helps stop bleeding and saves lives. However, according to the Centers for Disease Control and Prevention (CDC), about 60,000 to 100,000 Americans die each year from thrombosis, a disorder characterized by too much clotting. Blood clots can trigger a stroke or heart attack. According to X. Frank Zhang, associate professor in the Department of Bioengineering at Lehigh University, only one drug has been FDA-approved to target vWF and treat thrombosis, or excessive blood clotting disorders, Caplacizumab. It works by binding to vWF and blocking it from binding to platelets. However, no one has understood the specific mechanism behind how it accomplis

Busting Clots and Clearing Up A Chemical Mystery | Research Horizons | Georgia Tech s Research News

Posted April 12, 2021 • Atlanta, GA In a fortuitous case of mistaken chemical identity, a team of Georgia Tech bioengineers has discovered a promising new way to treat dangerous blood clots without the potentially harmful side effects of other clot-busting drugs. “It was a happy accident,” said David Ku, Regents’ professor in the George W. Woodruff School of Mechanical Engineering. “This is something we’ve been working on for the past four years, and we’re still sort of scratching our heads.” Ku and his collaborators explain their “happy accident” in the open access journal Their research is driven by the need for a better thrombolytic agent – a safer, more efficient treatment for breaking down clots in the immediate wake of a catastrophic event. When a clot develops in an artery – arterial thrombosis – it can stop the flow of blood to major organs, often leading to a stroke or heart attack. Depending on how it i

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