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

Complement System01:27

Complement System

2.7K
The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a...
2.7K
Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

909
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...
909
Venous Thrombosis III: Interprofessional Care01:29

Venous Thrombosis III: Interprofessional Care

22
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...
22
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

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

645
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...
645
Formation of the Platelet Plug01:22

Formation of the Platelet Plug

7.1K
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...
7.1K

You might also read

Related Articles

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

Sort by
Same author

Genetic screening of triple negative thrombocytosis patients identifies germline <i>MPL</i> compound mutations and <i>SH2B3/LNK</i> truncating mutations.

Haematologica·2026
Same author

Risk factors for acquisition of SARS-CoV-2 Omicron variant among a prospective cohort of French Healthcare Workers: impact of hybrid immunity.

Scientific reports·2026
Same author

Immune Profiling Identifies High-Risk Neutrophil-Rich Subtype in Checkpoint Inhibitor Nephritis.

Kidney international reports·2026
Same author

Complement involvement in antiphospholipid syndrome.

Immunology letters·2026
Same author

Thromboinflammation is associated with high thrombotic risk in patients with newly diagnosed myeloproliferative neoplasms.

Leukemia·2025
Same author

[Unusual bone marrow metastasis revealed by recurrent haematuria].

Annales de biologie clinique·2025

Related Experiment Video

Updated: Sep 12, 2025

Ferric Chloride-induced Murine Thrombosis Models
10:37

Ferric Chloride-induced Murine Thrombosis Models

Published on: September 5, 2016

22.0K

Complement in antiphospholipid syndrome, time to target?

Marie-Agnès Dragon Durey1, Houcine Hamidi2, Luc Darnige3

  • 1Laboratoire d'immunologie biologique, Hôpital Européen Georges Pompidou, APHP, Paris, France; INSERM UMRS 1138, team "Inflammation, Complement and Cancer", Cordeliers Research Center, Paris, France; Université de Paris Cité, Paris, France; University Hospital Federation (FHU) COMET, Paris, France.

Current Opinion in Immunology
|August 7, 2025
PubMed
Summary

Antiphospholipid syndrome (APS) involves complement system activation, yet its assessment isn't routine. Identifying biomarkers is crucial for evaluating new complement-targeting therapies in APS patients.

More Related Videos

A Fibrin-Enriched and tPA-Sensitive Photothrombotic Stroke Model
09:42

A Fibrin-Enriched and tPA-Sensitive Photothrombotic Stroke Model

Published on: June 4, 2021

2.9K
Methods for Quantitative Detection of Antibody-induced Complement Activation on Red Blood Cells
06:29

Methods for Quantitative Detection of Antibody-induced Complement Activation on Red Blood Cells

Published on: January 29, 2014

30.7K

Related Experiment Videos

Last Updated: Sep 12, 2025

Ferric Chloride-induced Murine Thrombosis Models
10:37

Ferric Chloride-induced Murine Thrombosis Models

Published on: September 5, 2016

22.0K
A Fibrin-Enriched and tPA-Sensitive Photothrombotic Stroke Model
09:42

A Fibrin-Enriched and tPA-Sensitive Photothrombotic Stroke Model

Published on: June 4, 2021

2.9K
Methods for Quantitative Detection of Antibody-induced Complement Activation on Red Blood Cells
06:29

Methods for Quantitative Detection of Antibody-induced Complement Activation on Red Blood Cells

Published on: January 29, 2014

30.7K

Area of Science:

  • Immunology
  • Hematology
  • Autoimmune Diseases

Background:

  • Antiphospholipid syndrome (APS) is an acquired autoimmune disorder characterized by thrombophilia.
  • The complement system, sharing components with the coagulation cascade, plays a significant role in APS pathophysiology.
  • Despite evidence of complement activation in APS patients (e.g., C4d, C3d, C5b9 fragments), its assessment is not standard clinical practice.

Purpose of the Study:

  • To highlight the established role of complement system activation in antiphospholipid syndrome.
  • To underscore the current gap in routine complement activation assessment for APS patients.
  • To emphasize the need for identifying biomarkers for novel complement-targeting therapies in APS.

Main Methods:

  • Review of existing literature on complement system involvement in APS.
  • Analysis of studies demonstrating complement activation fragments in APS patients and affected tissues.
  • Evaluation of current treatment strategies and emerging therapeutic targets.

Main Results:

  • Complement activation fragments (C4d, C3d, C5b9) are detected systemically and in affected tissues in APS.
  • Current standard treatment for APS involves long-term anticoagulation with vitamin K antagonists.
  • Case reports suggest potential efficacy of anti-C5 antibodies in severe APS forms, but more data is needed.

Conclusions:

  • Complement system activation is integral to antiphospholipid syndrome pathophysiology.
  • There is a clinical need for validated biomarkers to guide the use of complement-targeting therapies in APS.
  • Further research is required to establish the efficacy and role of complement inhibitors in APS management.