Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Anticoagulant Drugs: Low-Molecular-Weight Heparins

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...

Clot Retraction and Fibrinolysis

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.

Venous Thrombosis I: Introduction

Venous Thrombosis I: Introduction

Venous thrombosis, the most common disorder of the veins, involves the formation of a thrombus or blood clot associated with vein inflammation. It can be classified as either superficial vein thrombosis or deep vein thrombosis.Superficial Vein Thrombosis: This involves the formation of a thrombus in a superficial vein, usually the greater or lesser saphenous vein. Though less severe than deep vein thrombosis (DVT), SVT can lead to complications if untreated.Deep Vein Thrombosis (DVT): This...

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

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...

Intracellular Signaling Affects Focal Adhesions

Intracellular Signaling Affects Focal Adhesions

Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...

Extrinsic and Intrinsic Pathways of Hemostasis

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...

You might also read

Related Articles

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

Sort by

Same author

Correction: SCFβ-TRCP suppresses angiogenesis and thyroid cancer cell migration by promoting ubiquitination and destruction of VEGF receptor 2.

The Journal of experimental medicine·2025

Same author

Antiangiogenic Variant of TSP-1 Targets Tumor Cells in Glioblastomas.

Molecular therapy : the journal of the American Society of Gene Therapy·2024

Same author

Antiangiogenic Variant of TSP-1 Targets Tumor Cells in Glioblastomas.

Molecular therapy : the journal of the American Society of Gene Therapy·2024

Same author

The Tyrosine Kinase Inhibitor Lenvatinib Inhibits Anaplastic Thyroid Carcinoma Growth by Targeting Pericytes in the Tumor Microenvironment.

Thyroid : official journal of the American Thyroid Association·2023

Same author

Counter regulation of tumor angiogenesis by vascular endothelial growth factor and thrombospondin-1.

Seminars in cancer biology·2022

Same author

Addition of an Fc-IgG induces receptor clustering and increases the in vitro efficacy and in vivo anti-tumor properties of the thrombospondin-1 type I repeats (3TSR) in a mouse model of advanced stage ovarian cancer.

Gynecologic oncology·2021

Same journal

Fibrocytes drive JAK2V617F-mutated myelofibrosis: pitavastatin reverses marrow fibrosis and anemia.

Blood·2026

Same journal

Identifying steroid-refractory aGVHD before it happens.

Blood·2026

Same journal

ELISA-negative HIT: antibody recognition and relevance.

Blood·2026

Same journal

EBV and immunodeficiency: the odd couple drawn to the brain.

Blood·2026

Same journal

A bone to pick with ferric carboxymaltose.

Blood·2026

Same journal

A step toward streamlining HIT diagnosis.

Blood·2026

See all related articles

Search research articles

Related Experiment Video

Updated: Mar 14, 2026

A Fibrin-Enriched and tPA-Sensitive Photothrombotic Stroke Model

A Fibrin-Enriched and tPA-Sensitive Photothrombotic Stroke Model

Published on: June 4, 2021

When is a thrombogenic matrix not thrombogenic?

¹HARVARD MEDICAL SCHOOL.

|September 24, 2016

Summary

No abstract available in PubMed .

More Related Videos

Flow Cytometry Analysis of Tissue Factor Expression in Human Platelets

Flow Cytometry Analysis of Tissue Factor Expression in Human Platelets

Published on: November 22, 2024

Leveraging Turbidity and Thromboelastography for Complementary Clot Characterization

Leveraging Turbidity and Thromboelastography for Complementary Clot Characterization

Published on: June 4, 2020

Related Experiment Videos

Last Updated: Mar 14, 2026

A Fibrin-Enriched and tPA-Sensitive Photothrombotic Stroke Model

A Fibrin-Enriched and tPA-Sensitive Photothrombotic Stroke Model

Published on: June 4, 2021

Flow Cytometry Analysis of Tissue Factor Expression in Human Platelets

Flow Cytometry Analysis of Tissue Factor Expression in Human Platelets

Published on: November 22, 2024

Leveraging Turbidity and Thromboelastography for Complementary Clot Characterization

Leveraging Turbidity and Thromboelastography for Complementary Clot Characterization

Published on: June 4, 2020