Publications by authors named "Siyu M Chen"

Endothelial cells (ECs) normally form an anticoagulant surface under physiological conditions, but switch to support coagulation following pathogenic stimuli. This switch promotes thrombotic cardiovascular disease. To generate thrombin at physiologic rates, coagulation proteins assemble on a membrane containing anionic phospholipid, most notably phosphatidylserine (PS).

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Endothelial dysfunction accompanies the microvascular thrombosis commonly observed in severe COVID-19. Constitutively, the endothelial surface is anticoagulant, a property maintained at least in part via signaling through the Tie2 receptor. During inflammation, the Tie2 antagonist angiopoietin-2 (Angpt-2) is released from endothelial cells and inhibits Tie2, promoting a prothrombotic phenotypic shift.

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Profound endothelial dysfunction accompanies the microvascular thrombosis commonly observed in severe COVID-19. In the quiescent state, the endothelial surface is anticoagulant, a property maintained at least in part via constitutive signaling through the Tie2 receptor. During inflammation, the Tie2 antagonist angiopoietin-2 (Angpt-2) is released from activated endothelial cells and inhibits Tie2, promoting a prothrombotic phenotypic shift.

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Synopsis of recent research by authors named "Siyu M Chen"

  • - Siyu M Chen's research primarily focuses on the role of endothelial cells in coagulation and thrombosis, exploring how these cells transition from an anticoagulant state to a procoagulant one under pathological conditions, particularly in the context of cardiovascular diseases and COVID-19.
  • - Recent findings indicate that the protein TMEM16E has a significant role in regulating endothelial cell procoagulant activity and thrombosis, suggesting potential therapeutic targets for thrombotic cardiovascular diseases.
  • - Chen's work also highlights the protective effect of Tie2 receptor activation against prothrombotic endothelial dysfunction during severe COVID-19, revealing insights into the inflammatory processes that contribute to microvascular thrombosis.

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