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

Coagulation01:09

Coagulation

9.3K
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...
9.3K
Coagulation01:06

Coagulation

1.1K
Colloidal solids are solid particles suspended in solution. They are usually negatively charged, attracting a compact primary layer of positively charged ions, which attract more counterions to form an electrical double layer. Electrostatic repulsion between the charged double layers prevents the particles from colliding, stabilizing the colloids. These solids are often undesirable because they can contain toxins that are difficult to remove. Coagulation is a technique that helps aggregate and...
1.1K
Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

1.4K
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...
1.4K
Disorders of Hemostasis01:24

Disorders of Hemostasis

1.8K
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.
1.8K
Extrinsic and Intrinsic Pathways of Hemostasis01:20

Extrinsic and Intrinsic Pathways of Hemostasis

11.3K
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...
11.3K
Clot Retraction and Fibrinolysis01:16

Clot Retraction and Fibrinolysis

8.0K
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.
8.0K

You might also read

Related Articles

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

Sort by
Same author

Patient radiation exposure during invasive graft surveillance after heart transplantation.

Open heart·2026
Same author

Updating national diagnostic reference levels for adult cardiac interventional procedures in Switzerland.

Physica medica : PM : an international journal devoted to the applications of physics to medicine and biology : official journal of the Italian Association of Biomedical Physics (AIFB)·2026
Same author

Prognostic role of preoperative plasma fibrinogen-to-albumin ratio in urological carcinomas: a systematic review and meta-analysis.

BMC urology·2026
Same author

Reclassification of Exercise-Induced Arrhythmogenic Cardiomyopathy: Detection of a Pathogenic PKP2 Variant in a Male Athlete.

JACC. Case reports·2026
Same author

Remote Ischemic Postconditioning in Endovascular Thrombectomy for Stroke: The EnTRIPS Randomized Clinical Trial.

Stroke·2026
Same author

Electromagnetic interference during epicardial ablation in a patient with an extravascular implantable cardioverter-defibrillator and arrhythmogenic right ventricular cardiomyopathy: a case report.

European heart journal. Case reports·2026

Related Experiment Video

Updated: Dec 19, 2025

A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time
09:38

A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time

Published on: February 14, 2017

14.2K

Dysfunctional Coagulation in COVID-19: From Cell to Bedside.

Jie Wang1,2, Ardan M Saguner3, Jiaqi An4,5

  • 1Department of Cardiovascular Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, 277 Yanta West Road, Xi'an, 710061, China.

Advances in Therapy
|June 7, 2020
PubMed
Summary

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes COVID-19, leading to multisystem disease and dysfunctional coagulation. Understanding these mechanisms is crucial for developing effective anticoagulation therapies to reduce COVID-19 mortality.

Keywords:
ACE2COVID-19Dysfunctional coagulationSARS-CoV-2

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

1.1K
In Vitro Microfluidic Disease Model to Study Whole Blood-Endothelial Interactions and Blood Clot Dynamics in Real-Time
09:19

In Vitro Microfluidic Disease Model to Study Whole Blood-Endothelial Interactions and Blood Clot Dynamics in Real-Time

Published on: May 24, 2020

9.5K

Related Experiment Videos

Last Updated: Dec 19, 2025

A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time
09:38

A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time

Published on: February 14, 2017

14.2K
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

1.1K
In Vitro Microfluidic Disease Model to Study Whole Blood-Endothelial Interactions and Blood Clot Dynamics in Real-Time
09:19

In Vitro Microfluidic Disease Model to Study Whole Blood-Endothelial Interactions and Blood Clot Dynamics in Real-Time

Published on: May 24, 2020

9.5K

Area of Science:

  • Cardiovascular Medicine
  • Infectious Diseases
  • Hematology

Background:

  • Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, causing COVID-19, can result in multisystem disease.
  • Human angiotensin-converting enzyme 2 (ACE2) is a key receptor for SARS-CoV-2, and its dysfunction is implicated in COVID-19 pathogenesis.
  • Dysfunctional coagulation is a significant risk factor for severe COVID-19 and mortality.

Purpose of the Study:

  • To explore the mechanisms linking ACE2 dysfunction, endotheliitis, and innate immune responses to coagulation abnormalities in COVID-19.
  • To highlight the importance of understanding these mechanisms for developing effective anticoagulation strategies.

Main Methods:

  • Review of existing literature on SARS-CoV-2, ACE2 function, renin-angiotensin system, endotheliitis, and coagulation.
  • Analysis of the interplay between innate immunity, inflammation, and coagulation in COVID-19 patients.

Main Results:

  • ACE2 dysfunction contributes to renin-angiotensin system abnormalities and systemic endotheliitis.
  • Innate immune responses and inflammation play a role in the development of COVID-19-associated coagulopathy.
  • Dysfunctional coagulation is a critical factor in COVID-19 severity and fatality.

Conclusions:

  • Understanding the complex mechanisms of dysfunctional coagulation in COVID-19 is essential.
  • Targeting these mechanisms with appropriate anticoagulation therapies may improve patient outcomes and reduce mortality.