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A new study found that abnormal crosstalk between platelets and vascular intimal cells is one of the causes of fatal organ damage in patients with severe COVID-19
The study, led by researchers at New York University’s Grossman School of Medicine, revealed protein signals from platelets and cell fragments.
This study was published in the online edition of Science Advances on September 8.
In order to support the theory that platelets are the core of vascular damage in COVID-19, the research team also presented evidence that drugs (clopidogrel or ticagrelor) that block platelet activation through platelet surface protein P2Y12 are known to reduce COVID-19 related Inflammation of blood vessels
"Our findings reveal a new role in COVID-19 blood vessel damage, platelets, which may explain to a large extent the COVID-19 virus is more deadly than its relatives, causing the common cold," said corresponding author Tai · Dr.
Better understanding
The authors of the study said that abnormal systemic inflammation and blood clotting were identified as the core features of severe COVID-19 early in the pandemic, and the two are considered to be interrelated
In the current study, small blood vessel endothelial cells were exposed to the fluid released by platelets from COVID-19 patients or healthy similar patients (control group)
Through cross-comparison with the database, from the initial large list of potential culprits, the candidate list was reduced to two related genetic material fragments: S100A8 and S100A9, which coded for the construction of MRP 8 and 14
In addition, the research team also found that platelet-driven endothelial damage and abnormal coagulation may occur through the action of p-selectin in the platelet component alpha particles
Researchers also found that anticoagulant P2Y12 inhibitors reduced the expression of S100A8 and S100A9 in platelets by 18% within 4 weeks, preventing COVID-19 platelets from inducing vascular damage in laboratory tests
"The current research supports the theory that platelets activate endothelial cells through p-selectin.
Berger said that ACTIV-4a will also soon begin testing the effects of a p-selectin inhibitor called crizanlizumab in COVID-19 hospitalized patients
Original search:
Platelets Amplify Endotheliopathy in COVID-19
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