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

Venous Thrombosis I: Introduction01:30

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...
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...
Disorders of Hemostasis01:24

Disorders of Hemostasis

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.
Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...
Peripheral Artery Disease I: Introduction01:30

Peripheral Artery Disease I: Introduction

Peripheral artery disease (PAD) predominantly results from atherosclerosis, which involves the accumulation of fatty deposits, or plaques, within the walls of arteries. This causes them to narrow and harden, significantly reducing blood flow. PAD predominantly affects the legs, particularly the arteries supplying the thighs and calves. In rare cases, it may involve other arteries, including those in the arms.Etiology of PAD:The principal cause of PAD is atherosclerosis, which results from fatty...
Venous Thrombosis III: Interprofessional Care01:29

Venous Thrombosis III: Interprofessional Care

Venous thrombosis requires effective prevention and treatment strategies to improve patient outcomes and reduce potential complications.Prevention StrategiesHealthcare providers must prioritize preventing venous thromboembolism (VTE) for all adult patients upon admission. Interventions depend on bleeding and thrombosis risk, medical history, current medications, diagnoses, planned procedures, and patient preferences. Patients on bed rest should change positions every two hours and, if not...

You might also read

Related Articles

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

Sort by
Same author

Pharmacodynamics of Caplacizumab in Healthy Volunteers and Phase 2/3 Trial Patients with Immune-mediated Thrombotic Thrombocytopenic Purpura.

Thrombosis and haemostasis·2026
Same author

Commentary on "Endothelial Injury to Cognitive Decline: A 12-month Follow-up Using CT Perfusion and Diffusion MRI in Immune-mediated Thrombotic Thrombocytopenic Purpura".

Journal of thrombosis and haemostasis : JTH·2026
Same author

Daratumumab in relapse-refractory immune-mediated thrombotic thrombocytopenic purpura: additional evidence for its efficacy.

Research and practice in thrombosis and haemostasis·2026
Same author

Hemolytic Uremic Syndrome Outbreak in Adults and Shiga Toxin-Producing Escherichia coli Negative for Locus of Enterocyte Effacement, France, 2025.

Emerging infectious diseases·2026
Same author

Treating Immune-Mediated Thrombotic Thrombocytopenic Purpura with Caplacizumab.

Methods in molecular biology (Clifton, N.J.)·2026
Same author

Health-related quality of life in adults with von Willebrand disease: results of the French real-life Willebrand study on health-related quality of life.

Research and practice in thrombosis and haemostasis·2026

Related Experiment Video

Updated: Jun 25, 2026

Thrombus Profiling Assay: A Microfluidics-Based Platform for Comprehensively Characterizing Biomechanical Thrombogenesis
08:50

Thrombus Profiling Assay: A Microfluidics-Based Platform for Comprehensively Characterizing Biomechanical Thrombogenesis

Published on: January 9, 2026

Thrombotic microangiopathies: towards a pathophysiology-based classification.

Paul Coppo1, Agnès Veyradier

  • 1Service d'Hématologie et de Thérapie Cellulaire, Hôpital Saint-Antoine, 184 rue du Fbg St Antoine 75012 Paris, France. paulcoppo@aol.com

Cardiovascular & Hematological Disorders Drug Targets
|March 12, 2009
PubMed
Summary

Thrombotic microangiopathies (TMA) are serious conditions involving blood clots and organ failure. Understanding their molecular basis, like ADAMTS13 deficiency in TTP and complement issues in HUS, enables targeted therapies.

More Related Videos

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

Endothelialized Microfluidics for Studying Microvascular Interactions in Hematologic Diseases
11:08

Endothelialized Microfluidics for Studying Microvascular Interactions in Hematologic Diseases

Published on: June 22, 2012

Related Experiment Videos

Last Updated: Jun 25, 2026

Thrombus Profiling Assay: A Microfluidics-Based Platform for Comprehensively Characterizing Biomechanical Thrombogenesis
08:50

Thrombus Profiling Assay: A Microfluidics-Based Platform for Comprehensively Characterizing Biomechanical Thrombogenesis

Published on: January 9, 2026

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

Endothelialized Microfluidics for Studying Microvascular Interactions in Hematologic Diseases
11:08

Endothelialized Microfluidics for Studying Microvascular Interactions in Hematologic Diseases

Published on: June 22, 2012

Area of Science:

  • Hematology
  • Pathophysiology
  • Immunology

Background:

  • Thrombotic microangiopathies (TMA) are a group of disorders characterized by microangiopathic hemolytic anemia, thrombocytopenia, and organ damage.
  • Thrombotic thrombocytopenic purpura (TTP) involves severe systemic organ failure due to deficient ADAMTS13 activity, leading to uncleaved von Willebrand factor multimers.
  • Hemolytic uremic syndrome (HUS) primarily presents with renal failure, often linked to Shiga toxin-producing E. coli or complement pathway dysregulation in atypical HUS.

Purpose of the Study:

  • To elucidate the pathophysiology of various TMA syndromes.
  • To highlight the role of ADAMTS13 deficiency in TTP and complement pathway dysfunction in atypical HUS.
  • To emphasize the potential for molecular classification and targeted therapies in TMA.

Main Methods:

  • Review of existing literature on TMA pathophysiology.
  • Analysis of genetic and immunological factors contributing to TTP and HUS.
  • Discussion of diagnostic criteria and therapeutic approaches.

Main Results:

  • TTP pathogenesis is linked to ADAMTS13 deficiency, caused by genetic mutations or autoantibodies, with autoimmune associations in acquired TTP.
  • Atypical HUS is associated with genetic defects in complement regulatory proteins (Factor H, I, CD46, Factor B, C3).
  • Advances in understanding TMA mechanisms facilitate molecular classification.

Conclusions:

  • Accurate molecular classification of TMA syndromes is now achievable.
  • Improved understanding paves the way for novel, targeted therapeutic strategies for TTP and HUS.
  • TMA represents a complex group of diseases requiring a multi-faceted diagnostic and therapeutic approach.