Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

672
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...
672
Extrinsic and Intrinsic Pathways of Hemostasis01:20

Extrinsic and Intrinsic Pathways of Hemostasis

7.0K
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...
7.0K
Clot Retraction and Fibrinolysis01:16

Clot Retraction and Fibrinolysis

5.4K
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.
5.4K
Disorders of Hemostasis01:24

Disorders of Hemostasis

824
Hemostasis, the process that stops bleeding after a blood vessel injury, is crucial for maintaining the integrity of the circulatory system. However, disorders of hemostasis can disrupt this delicate balance, leading to either excessive clotting or bleeding. These disorders can be broadly classified into thromboembolic disorders and bleeding disorders.
Thromboembolic Disorders
Two factors primarily cause thromboembolic conditions.
824
Formation of the Platelet Plug01:22

Formation of the Platelet Plug

5.7K
The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
5.7K
Coagulation01:09

Coagulation

6.1K
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...
6.1K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Towards Personalized Therapy of Aortic Stenosis.

Journal of personalized medicine·2021
Same author

Challenges for Polish Archives of Internal Medicine in 2021: what is new in 2022?

Polish archives of internal medicine·2021
Same author

Direct oral anticoagulants in patients with atrial fibrillation following bariatric surgery: A single center experience.

Kardiologia polska·2021
Same author

[Teaching Evidence Based Medicine EBM in medical faculties in Poland].

Polski merkuriusz lekarski : organ Polskiego Towarzystwa Lekarskiego·2021
Same author

Fibrinogen β chain and FXIII polymorphisms affect fibrin clot properties in acute pulmonary embolism.

European journal of clinical investigation·2021
Same author

Fibrin clot properties and fibrinolysis in patients with endocrine hypertension due to aldosterone or catecholamines excess.

Clinical endocrinology·2021

Related Experiment Video

Updated: Jun 21, 2025

Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay
13:08

Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay

Published on: September 9, 2012

18.9K

Elevated plasma factor XI is associated with postthrombotic syndrome.

Konrad Stępień1, Jakub Siudut2, Jarosław Zalewski3

  • 1Department of Thromboembolic Disorders, Institute of Cardiology, Jagiellonian University Medical College, Krakow, Poland; Department of Coronary Artery Disease and Heart Failure, St. John Paul II Hospital, Krakow, Poland.

Thrombosis Research
|July 5, 2024
PubMed
Summary
This summary is machine-generated.

Elevated Factor XI (FXI) levels are linked to postthrombotic syndrome (PTS) development after deep vein thrombosis (DVT). Higher FXI is associated with PTS occurrence, recurrence, and venous ulcers, suggesting its role in DVT complications.

Keywords:
Factor XIFibrin clotPostthrombotic syndromeThrombin generationVenous thromboembolism

More Related Videos

Author Spotlight: Deciphering Coagulation Disorders in Traumatic Brain Injury Patients
04:56

Author Spotlight: Deciphering Coagulation Disorders in Traumatic Brain Injury Patients

Published on: August 4, 2023

734
Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
04:37

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation

Published on: May 23, 2025

330

Related Experiment Videos

Last Updated: Jun 21, 2025

Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay
13:08

Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay

Published on: September 9, 2012

18.9K
Author Spotlight: Deciphering Coagulation Disorders in Traumatic Brain Injury Patients
04:56

Author Spotlight: Deciphering Coagulation Disorders in Traumatic Brain Injury Patients

Published on: August 4, 2023

734
Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
04:37

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation

Published on: May 23, 2025

330

Area of Science:

  • Hematology
  • Vascular Biology
  • Thrombosis Research

Background:

  • Postthrombotic syndrome (PTS) is a frequent complication of deep vein thrombosis (DVT).
  • PTS pathogenesis involves inflammatory and prothrombotic mechanisms.
  • The specific role of Factor XI (FXI) in PTS has not been previously investigated.

Purpose of the Study:

  • To investigate the association between elevated Factor XI (FXI) levels and the occurrence of postthrombotic syndrome (PTS) in patients with deep vein thrombosis (DVT).

Main Methods:

  • 180 patients with a first-ever DVT were enrolled.
  • Factor XI (FXI) levels, inflammatory markers, thrombin generation, clot permeability (Ks), clot lysis time (CLT), and fibrinolysis proteins were measured after 3 months.
  • PTS was assessed using the Villalta score, with follow-up for venous thromboembolism (VTE) recurrence and venous ulcers.

Main Results:

  • Patients with PTS exhibited significantly higher FXI levels compared to those without PTS.
  • Elevated FXI (≥120%) was more frequent in PTS patients, showing a strong association (OR 5.55).
  • Higher baseline FXI independently predicted PTS occurrence and VTE recurrence, and was linked to venous ulcers at long-term follow-up.

Conclusions:

  • Elevated Factor XI (FXI) is independently associated with postthrombotic syndrome (PTS) development after deep vein thrombosis (DVT).
  • FXI's association with inflammation and altered clot properties may contribute to PTS pathogenesis.
  • These findings highlight FXI as a potential therapeutic target for preventing PTS.