Related Experiment Video

Updated: Oct 20, 2025

Investigating von Willebrand Factor Pathophysiology Using a Flow Chamber Model of von Willebrand Factor-platelet String Formation
08:30

Investigating von Willebrand Factor Pathophysiology Using a Flow Chamber Model of von Willebrand Factor-platelet String Formation

Published on: August 14, 2017

11.4K

Von Willebrand factor: A key glycoprotein involved in thrombo-inflammatory complications of COVID-19

Shalki Choudhary1, Kajal Sharma1, Pankaj Kumar Singh2

  • 1Molecular Modeling Lab (MML), Department of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala, Punjab, 147002, India.

Chemico-Biological Interactions
|September 13, 2021
PubMed

Insights

Von Willebrand Factor (VWF) is crucial in COVID-19-related thrombo-inflammation and acute respiratory distress syndrome (ARDS). Targeting VWF may help manage severe COVID-19 complications and improve patient outcomes.

Area of Science:

  • Cardiovascular Medicine
  • Infectious Diseases
  • Hematology

Background:

  • COVID-19 triggers endothelial cell activation, disrupting vascular integrity and promoting inflammation and coagulation.
  • A significant link exists between coagulation and inflammatory pathways in COVID-19 pathophysiology.
  • Thrombo-inflammatory complications like hypercoagulation, thrombosis, and ARDS are leading causes of mortality in severe COVID-19 cases.

Purpose of the Study:

  • To explore the role of Von Willebrand Factor (VWF) in COVID-19 pathophysiology.
  • To investigate VWF as a potential therapeutic target for managing COVID-19-associated thrombo-inflammation and comorbidities.
  • To summarize current knowledge on VWF's mechanism, diagnosis, and management in COVID-19.

Main Methods:

  • Literature review and synthesis of existing research on VWF in COVID-19.
  • Analysis of pathophysiological mechanisms linking VWF to COVID-19 complications.
  • Exploration of VWF's role as a coagulation biomarker and therapeutic target.

Main Results:

  • Von Willebrand Factor (VWF) is identified as a key mediator in COVID-19-associated thrombo-inflammation.
  • VWF's involvement in vascular inflammation and coagulation contributes to severe outcomes like ARDS.
  • Previous research indicates VWF targeting is effective for thrombo-inflammation in other conditions.

Conclusions:

  • Von Willebrand Factor (VWF) presents a promising target for therapeutic intervention in COVID-19.
  • Understanding VWF's role is critical for developing strategies to mitigate COVID-19-related mortality.
  • Further research into VWF as a biomarker and therapeutic target in COVID-19 is warranted.

Keywords:
COVID-19Pulmonary embolismSARS-CoV-2Thrombo-inflammatory complicationsVon willebrand factor

More Related Videos

In Vitro and In Vivo Model to Study Bacterial Adhesion to the Vessel Wall Under Flow Conditions10:24

In Vitro and In Vivo Model to Study Bacterial Adhesion to the Vessel Wall Under Flow Conditions

Published on: June 11, 2015

10.9K
Pneumococcus Infection of Primary Human Endothelial Cells in Constant Flow09:34

Pneumococcus Infection of Primary Human Endothelial Cells in Constant Flow

Published on: October 31, 2019

6.7K

Related Concept Videos

Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
1.1K
Extrinsic and Intrinsic Pathways of Hemostasis01:20

Extrinsic and Intrinsic Pathways of Hemostasis

Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which...
10.1K
Structure and Function of Platelets01:18

Structure and Function of Platelets

The cell fragments known as platelets are disc-shaped, with an average diameter of about 3 μm and a thickness of roughly 1 μm. They play a crucial role in the body's vascular clotting system, which also involves plasma proteins, blood cells, and blood vessel tissues.
Platelets are continually replenished, circulating in the bloodstream for 9-12 days before being removed by phagocytes, primarily in the spleen. A microliter of circulating blood contains between 150,000 and 450,000...
2.2K
Coagulation01:09

Coagulation

The coagulation phase is a critical part of the body's process to prevent blood loss following injury to blood vessels. It involves chemical reactions that form a clot to seal the injured area. The clotting process begins shortly after injury, within 15-20 seconds for severe damage and 1-2 minutes for minor injuries.
During the coagulation phase, clotting factors, or procoagulants, play a vital role in initiating and progressing the coagulation cascade. This cascade is a series of reactions...
8.1K
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
764
Clot Retraction and Fibrinolysis01:16

Clot Retraction and Fibrinolysis

After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
7.5K