Platelets key to blood vessel damage in COVID-19 patients

platelets key to blood vessel damage in covid 19 patients

Sumary of Platelets key to blood vessel damage in COVID-19 patients:

  • Abnormal crosstalk between blood platelets and cells lining blood vessels is one cause of deadly organ damage in patients with severe COVID-19, a new study finds.
  • Led by researchers from NYU Grossman School of Medicine, the study revealed the protein signals given off by platelets, cell fragments that contribute to blood clotting, create inflammation, abnormal clotting, and damage to vessels when exposed to the pandemic virus.
  • In support of the theory that platelets are at the core of blood vessel damage in COVID-19, the research team also presented evidence that approved medications known to block platelet activation via the platelet surface protein P2Y12 (clopidogrel or ticagrelor) reduced COVID-19-related inflammation in vessels.
  • The study also found that COVID-19-exposed platelets change cells lining blood vessels (endothelial cells) largely through a protein called P-selectin, which makes platelets stickier and more likely to form clots.
  • “Our findings reveal a new role for platelets in COVID-19 blood vessel damage, and may explain in large part what makes the COVID-19 virus so much more deadly than its relatives that cause the common cold,” says corresponding author Tessa Barrett, PhD, research assistant professor in the Department of Medicine at NYU Langone Health.
  • Better Understanding Abnormal, body-wide inflammation and blood clotting were identified early in the pandemic as central features of severe COVID-19, with the two thought to be interrelated, say the study authors.
  • As blood components that react to injuries in vessels by triggering inflammation, and by becoming sticky to clump together in clots, platelets have been suggested as a culprit for the observed damage.
  • Further, evidence is mounting that the interplay between platelets and endothelial cells may be important to these disease mechanisms.

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